Database Query Results : Quercetin, ,

QC, Quercetin: Click to Expand ⟱
Features:
Plant pigment (flavonoid) found in red wine, onions, green tea, apples and berries.
Quercetin is thought to contribute to anticancer effects through several mechanisms:
-Antioxidant Activity:
-Induction of Apoptosis:modify Bax:Bcl-2 ratio
-Anti-inflammatory Effects:
-Cell Cycle Arrest:
-Inhibition of Angiogenesis and Metastasis: (VEGF)

Cellular Pathways:
-PI3K/Akt/mTOR Pathway: central to cell proliferation, survival, and metabolism.
-MAPK/ERK Pathway: influencing cell proliferation, differentiation, and apoptosis.
-NF-κB Pathway: downregulate NF-κB
-JAK/STAT Pathway: interfere with the activation of STAT3
-Apoptotic Pathways: intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways

Quercetin has been used at doses around 500–1000 mg per day
Quercetin’s bioavailability from foods or standard supplements can be low.

-Note half-life 11 to 28 hours.
BioAv low 1-10%, poor water-solubility, consuming with fat may improve bioavialability. also piperine or VitC.
Pathways:
- induce ROS production in cancer cells (higher dose). Typicallys Lowers ROS in normal cells(unless it is high dose?)or depends on Redox status?. "quercetin paradox"
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Confusing info about Lowering AntiOxidant defense in Cancer Cells: NRF2↓(some contrary), TrxR↓**, SOD↓(contrary), GSH↓ Catalase↓(contrary), HO1↓(some contrary), GPx↓(some contrary)
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓,
- some indication of inhibiting Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD24↓, β-catenin↓, Notch2↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS Conditional Driver Biphasic redox modulation Quercetin exhibits pro-oxidant behavior in cancer cells while protecting normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction is a central apoptosis route in cancer cells
3 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Driver Growth and survival inhibition AKT/mTOR suppression is a consistently reported upstream effect in cancer models
4 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Reduced survival and inflammatory transcription NF-κB inhibition contributes to chemosensitization and apoptosis susceptibility
5 MAPK signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-mediated apoptosis signaling MAPK activation supports apoptosis downstream of redox stress
6 Cell cycle regulation ↑ G1/S or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects disruption of growth signaling
7 HIF-1α hypoxia signaling ↓ HIF-1α ↔ minimal Secondary Reduced hypoxia tolerance Quercetin interferes with hypoxia-driven transcriptional programs
8 NRF2 antioxidant response ↑ NRF2 (adaptive, context-dependent) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 induction reflects redox buffering rather than primary cytotoxicity


Scientific Papers found: Click to Expand⟱
380- AgNPs,  QC,  CA,  Chit,    Quercetin- and caffeic acid-functionalized chitosan-capped colloidal silver nanoparticles: one-pot synthesis, characterization, and anticancer and antibacterial activities
- in-vitro, MG, U118MG
"highlight2" >TumCG↓, cell viability has constantly decreased by increasing the concentration

6- Ba,  Api,  QC,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, PC3
"highlight2" >HH↓, Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
"highlight2" >Gli1↓, three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA concentration but not Gli reporter activity

3633- BBR,  LT,  Cro,  QC,    Naturally Occurring Acetylcholinesterase Inhibitors and Their Potential Use for Alzheimer's Disease Therapy
- Review, AD, NA
"highlight2" >*AChE↓, Alzheimer's disease (AD) is a main cause of dementia, accounting for up to 75% of all dementia cases. Pathophysiological processes described for AD progression involve neurons and synapses degeneration, mainly characterized by cholinergic impairment.
"highlight2" >*AChE↓, Fig1: Berberine(1uM), Luteolin(80uM), Crocetin(100uM), Quercetin(120uM)

24- EGCG,  GEN,  QC,    Targeting CWR22Rv1 prostate cancer cell proliferation and gene expression by combinations of the phytochemicals EGCG, genistein and quercetin
- in-vitro, Pca, 22Rv1
"highlight2" >NQO1↑, Genistein and quercetin, as individual phytochemicals, increased NQO1 expression by ~3.78- and ~6.42-fold, respectively,
"highlight2" >P53↑, Taken together, these results support the existence of synergy between EGCG, genistein and quercetin in the control of AR, p53 and NQO1 expression
"highlight2" >NQO2↑,
"highlight2" >chemoPv↑, synergy between bioactive dietary agents, thus broadening the chemopreventive index
"highlight2" >TumCP↓, Analyzing the results from colony formation and cell proliferation together, the relative potency and efficacy of the three phytochemicals was ranked as EGCG>quercetin>genistein.
"highlight2" >AR↓, EGCG or quercetin (2.5 μM) separately, inhibited AR expression by 67% and 47%, respectively compared to the control,

25- EGCG,  QC,    Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
"highlight2" >COMT↓, fact that EGCG primarily inhibited COMT activity, whereas quercetin reduced the amount of COMT protein.
"highlight2" >TumCP↑, Quercetin and EGCG in combination synergistically inhibited cell proliferation, caused cell cycle arrest, and induced apoptosis in PC-3 cells.
"highlight2" >TumCCA↑,
"highlight2" >Apoptosis↑,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
"highlight2" >BAD↓,
"highlight2" >cl‑PARP↑,
"highlight2" >Casp7↑,
"highlight2" >IκB↓,
"highlight2" >Ki-67↓,
"highlight2" >VEGF↓,
"highlight2" >EGFR↓,
"highlight2" >FGF↓,
"highlight2" >TGF-β↓,
"highlight2" >TNF-α↓,
"highlight2" >SCF↓,
"highlight2" >Bax:Bcl2↑,
"highlight2" >NF-kB↓,
"highlight2" >chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
"highlight2" >ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
"highlight2" >TumVol↓,

2458- EGCG,  QC,    Identification of plant-based hexokinase 2 inhibitors: combined molecular docking and dynamics simulation studies
- Analysis, Nor, NA
"highlight2" >HK2↓, Overall, this study concludes that EGCG and quercitrin might possess the inhibitory potential for HK2.

2642- Flav,  QC,  Api,  KaempF,  MCT  In Vitro–In Vivo Study of the Impact of Excipient Emulsions on the Bioavailability and Antioxidant Activity of Flavonoids: Influence of the Carrier Oil Type
- in-vitro, Nor, NA - in-vivo, Nor, NA
"highlight2" >*BioAv↑, Overall, the bioavailability and antioxidant activity of flavonoids increased when they were coingested with excipient emulsions.
"highlight2" >*eff↝, However, in vivo pharmacokinetic experiments showed that the flavonoid concentrations in rat serum were comparable for all carrier oils
"highlight2" >BioEnh↑, MCT is the bioenhancer for the Flavonoids (which have low soluability in water)

4687- LT,  QC,    Dietary Flavonoids Luteolin and Quercetin Suppressed Cancer Stem Cell Properties and Metastatic Potential of Isolated Prostate Cancer Cells
- in-vitro, Pca, DU145
"highlight2" >CSCs↓, Since luteolin and quercetin were able to target CSC cells and prevent cancer cell invasiveness, may serve as potential anti-angiogenesis and anti-metastasis agents.
"highlight2" >EMT↓, Furthermore, reversed epithelial-mesenchymal transition (EMT) to reduce MMP secretion by Lu and Qu exert inhibition of migration and invasion abilities in A431 cells
"highlight2" >MMPs↓,
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,

1997- Myr,  QC,    Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity
- in-vitro, Lung, A549
"highlight2" >TrxR↓, Myricetin and quercetin were found to have strong inhibitory effects on mammalian TrxRs with IC50 values of 0.62 and 0.97 micromol/L, respectively
"highlight2" >eff↑, Oxygen-derived superoxide anions enhanced the inhibitory effect whereas anaerobic conditions attenuated inhibition.
"highlight2" >TumCCA↑, cell cycle was arrested in S phase by quercetin and an accumulation of cells in sub-G1 was observed in response to myricetin.
"highlight2" >eff↓, presence of superoxide dismutase diminished the inhibition dramatically
"highlight2" >ROS↑, show that ROS played a critical role in the inhibition of TrxR by flavonoids. ...may occur as a result of their easy oxidization to flavonol semiquinone species.

981- NarG,  QC,    Anti-estrogenic and anti-aromatase activities of citrus peels major compounds in breast cancer
- in-vivo, NA, NA
"highlight2" >TumVol↓,
"highlight2" >CYP19↓, Reduction in aromatase levels in solid tumors was also observed in treated groups (Aromatase inhibitor)

910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
"highlight2" >tumCV↓,
"highlight2" >Apoptosis↑,
"highlight2" >PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
"highlight2" >Wnt/(β-catenin)↓, reducing β-catenin
"highlight2" >MAPK↝,
"highlight2" >ERK↝, ERK1/2
"highlight2" >TumCCA↑, cell cycle arrest at the G1 phase
"highlight2" >H2O2↑,
"highlight2" >ROS↑,
"highlight2" >TumAuto↑,
"highlight2" >MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
"highlight2" >P53↑,
"highlight2" >Casp3↑,
"highlight2" >Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
"highlight2" >cFLIP↓,
"highlight2" >IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
"highlight2" >IL10↓,
"highlight2" >lactateProd↓,
"highlight2" >Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
"highlight2" >PKM2↓,
"highlight2" >GLUT1↓,
"highlight2" >COX2↓,
"highlight2" >VEGF↓,
"highlight2" >OCR↓,
"highlight2" >ECAR↓,
"highlight2" >STAT3↓,
"highlight2" >MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
"highlight2" >MMP9:TIMP1↓,
"highlight2" >mTOR↓,

911- QC,  SFN,    Pilot study evaluating broccoli sprouts in advanced pancreatic cancer (POUDER trial) - study protocol for a randomized controlled trial
"highlight2" >TumCG↓,
"highlight2" >Risk↓, decreased risk of extra-prostatic manifestation of prostate cancer: cruciferous vegetables, in particular broccoli which is rich in sulforaphane and quercetin

909- QC,    Exploring the therapeutic potential of quercetin in cancer treatment: Targeting long non-coding RNAs
- Review, NA, NA
"highlight2" >other↓, quercetin suppresses oncogenic lncRNAs
"highlight2" >other↑, while enhancing tumor-suppressive lncRNAs

908- QC,    Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update
- Review, NA, NA
"highlight2" >AntiCan↑, quercetin exerts anticancer effect by binding to cellular receptors and proteins
"highlight2" >ROS↑, The short-term effect causes scavenging of free radicals and it is mostly antioxidative and antiapoptotic in nature, while the long term effect is pro-oxidative

907- QC,    A Comprehensive Study on the Anti-cancer Effects of Quercetin and Its Epigenetic Modifications in Arresting Progression of Colon Cancer Cell Proliferation
- Review, NA, NA
"highlight2" >AntiCan↑, fascinated attention to quercetin as an anti-inflammatory plant product since it exerts specific effects only on cancer cells rather than on normal

906- QC,    The interplay between reactive oxygen species and antioxidants in cancer progression and therapy: a narrative review
- Review, NA, NA
"highlight2" >ROS↑, quercetin at higher concentrations (>50 µM) can initiate ROS generation especially O2•−

905- QC,    Anti- and pro-oxidant effects of quercetin in copper-induced low density lipoprotein oxidation. Quercetin as an effective antioxidant against pro-oxidant effects of urate
- Analysis, NA, NA
"highlight2" >ROS↑, pro-oxidant behavior depends on the Cu(2+) concentration

904- QC,    Antioxidant and prooxidant effects of quercetin on glyceraldehyde-3-phosphate dehydrogenase
- Analysis, NA, NA
"highlight2" >ROS↑, Quercetin significantly increased oxidation of GAPDH observed in the presence of ferrous ions
"highlight2" >H2O2↑,

903- QC,    Potential toxicity of quercetin: The repression of mitochondrial copy number via decreased POLG expression and excessive TFAM expression in irradiated murine bone marrow
- in-vivo, NA, NA
"highlight2" >ROS⇅, antioxidant and prooxidant effects largely relates to its dose

902- QC,    Prooxidant activities of quercetin, p-courmaric acid and their derivatives analysed by quantitative structure–activity relationship
- Analysis, NA, NA
"highlight2" >ROS↑, metal ion and concentration of tested phenolics are widely suggested to affect the prooxidant activity of phenolics

901- QC,    Antioxidant/prooxidant effects of α-tocopherol, quercetin and isorhamnetin on linoleic acid peroxidation induced by Cu(II) and H2O2
- Analysis, Var, NA
"highlight2" >ROS↑, presence/ absence of metal ions modulates the biological or pharmacological behavior of flavonoids to act as an antioxidant or prooxidant

900- QC,    Quercetin Affects Erythropoiesis and Heart Mitochondrial Function in Mice
- in-vivo, Nor, NA
"highlight2" >*Weight↓, overall weight
"highlight2" >*TAC∅, no significant decrease
"highlight2" >*ROS↑, working hypothesis is that quercetin interferes with mitochondrial function exacerbating mitochondrial ROS generation and altering the physiology of tissues highly dependent on iron metabolism

99- QC,    Quercetin Inhibits Epithelial-to-Mesenchymal Transition (EMT) Process and Promotes Apoptosis in Prostate Cancer via Downregulating lncRNA MALAT1
- in-vitro, Pca, PC3
"highlight2" >EMT↓, quercetin suppressed EMT process, promote apoptosis and deactivated PI3K/Akt signaling pathway in PC-3 cells
"highlight2" >E-cadherin↑, Quercetin increased E-cadherin expression and decreased the level of N-cadherin
"highlight2" >N-cadherin↓,
"highlight2" >Ki-67↓, while the production of Ki67 was significantly reduced by quercetin
"highlight2" >PI3K/Akt↓,
"highlight2" >MALAT1↓, MALAT1 expression was significantly downregulated in quercetin-treated PC cells at a dose- and time-dependent manne
"highlight2" >TumCG↓, Quercetin Inhibited Tumor Growth by Targeting MALAT1 in vivo

912- QC,  2DG,    Selected polyphenols potentiate the apoptotic efficacy of glycolytic inhibitors in human acute myeloid leukemia cell lines. Regulation by protein kinase activities
"highlight2" >Apoptosis↑,
"highlight2" >ROS↓, 2-DG (5 mM) and Quer (10–40 μM) reduced the basal intracellular ROS content in HL60 cells
"highlight2" >GSH∅, GSH levels were not significantly affected by treatment for 3 h
"highlight2" >other↑, activated apoptosis throughout the mitochondrial (“intrinsic”) executioner pathway

899- QC,    Intracellular metabolism and bioactivity of quercetin and its in vivo metabolites
- in-vivo, Var, NA
"highlight2" >ROS↑, effects of quercetin on cells seem to be dependent both on cell type and in particular on the concentration of quercetin
"highlight2" >GSH↓,

898- QC,    Anti- and pro-oxidant activity of rutin and quercetin derivatives
- Analysis, Var, NA
"highlight2" >ROS↑, quercetin derivatives with free catechol moiety or free hydroxyl in position 3 (or both) were pro-oxidant

897- QC,    Anti- and prooxidant effects of chronic quercetin administration in rats
- in-vivo, Nor, NA
"highlight2" >*MDA↓, in rat livers (decrease was more pronounced in vitamin E-deprived rats)
"highlight2" >*GSH⇅, in liver
"highlight2" >*ROS⇅, results suggest that quercetin may act not only as an antioxidant, but also as a prooxidant in rats.

896- QC,    Antioxidant and pro-oxidant actions of the plant phenolics quercetin, gossypol and myricetin: Effects on lipid peroxidation, hydroxyl radical generation and bleomycin-dependent damage to DNA
- in-vivo, Var, NA
"highlight2" >ROS↑, Hence these naturally-occurring substances can have pro-oxidant effects under some reaction conditions and cannot be classified simplistically as “antioxidants”.

895- QC,    Theoretical Study of the Antioxidant Activity of Quercetin Oxidation Products
- Analysis, Var, NA
"highlight2" >ROS⇅,

894- QC,    The antioxidant, rather than prooxidant, activities of quercetin on normal cells: quercetin protects mouse thymocytes from glucose oxidase-mediated apoptosis
- in-vitro, Nor, NA
"highlight2" >Apoptosis↑, capable of inducing apoptosis in tumor cell
"highlight2" >*NF-kB↓, the G/GO-mediated increase in NF-kB activity was clearly inhibited when the cells were pretreated with 50uM quercetin
"highlight2" >*AP-1↓, activation is suppressed by quercetin treatment.
"highlight2" >*P53↝, G/GO-mediated oxidative stress activates nuclear translocation and activation of the wild-type p53 in thymocytes and that this activation is inhibited by quercetin.
"highlight2" >*ROS↓, normal mouse thymocytes glucose oxidase stress

893- QC,    Quercetin: Prooxidant Effect and Apoptosis in Cancer
- Analysis, Var, NA
"highlight2" >ROS↑, proposal that the capacity of quercetin as a phytochemical that is able to trigger apoptosis in several tumor cell lineages might be related to its prooxidant features.

892- QC,    Antioxidant vs. pro-oxidant activities of quercetin in aqueous phase: A Density Functional Theory study
- Analysis, Var, NA
"highlight2" >ROS↑, influenced by concentration, pH of environment and the presence of redox metal.

891- QC,    Chapter 9 - Quercetin: Prooxidant Effect and Apoptosis in Cancer
- in-vitro, Var, NA
"highlight2" >ROS↑, substantial evidence that its prooxidant features are also relevant regarding its tumoricidal effects
"highlight2" >AntiTum↑, promote tumoricidal effects.

890- QC,    PROOXIDANT ACTIVITIES OF ANTIOXIDANTS AND THEIR IMPACT ON HEALTH
- Review, Var, NA
"highlight2" >ROS↑, in the presence of the transition metal

889- QC,    The multifaceted role of quercetin derived from its mitochondrial mechanism
- vitro+vivo, Var, NA
"highlight2" >MMP↓,
"highlight2" >ATP↝,
"highlight2" >OXPHOS↝,
"highlight2" >ROS↑, a prooxidant effect

873- QC,  RES,  CUR,  PI,    Combination Effects of Quercetin, Resveratrol and Curcumin on In Vitro Intestinal Absorption
- in-vitro, Nor, NA
"highlight2" >*BioEnh↑, Resveratrol received the greatest enhancement in permeability when combined with other agents: quercetin (310%), curcumin (300%), quercetin and curcumin (323%, 350% with piperine)

138- QC,  CUR,    Sensitization of androgen refractory prostate cancer cells to anti-androgens through re-expression of epigenetically repressed androgen receptor - Synergistic action of quercetin and curcumin
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
"highlight2" >DNMTs↓, treatment with Q+C was much more effective than either Q or C in inhibiting DNMT,
"highlight2" >AR↑, Treatment with Q or C or Q+C resulted in a marked increase in the expression of AR protein levels in PC3 and DU145 cell lines,
"highlight2" >MMP↓, combined treatment with Q+C was stronger than that of individual treatments (Q or C) in depolarizing the mitochondrial membrane potential

100- QC,    Inhibition of Prostate Cancer Cell Colony Formation by the Flavonoid Quercetin Correlates with Modulation of Specific Regulatory Genes
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
"highlight2" >cycD1/CCND1↓, CCND1, CCND2, CCND3
"highlight2" >cycE/CCNE↓, CCNE1, CCNE2
"highlight2" >CDK2↓,
"highlight2" >CDK4/6↓, CDK4, CDK8
"highlight2" >E2Fs↓, E2F2, E2F3
"highlight2" >PCNA↓,
"highlight2" >cDC2↓,
"highlight2" >PTEN↑,
"highlight2" >MSH2↑,
"highlight2" >P21↑,
"highlight2" >EP300↑, p300
"highlight2" >BRCA1↑,
"highlight2" >NF2↑,
"highlight2" >TSC1↑,
"highlight2" >TGFβR1↑, TGFβR2
"highlight2" >P53↑,
"highlight2" >RB1↑, Rb
"highlight2" >AKT1↓,
"highlight2" >cMyc↓,
"highlight2" >CDC7↓,
"highlight2" >cycF↓, CCNF
"highlight2" >CDC16↓,
"highlight2" >CUL4B↑, CUL4B, a member of the cullin gene family that is also known to be involved in control of the cell cycle, was significantly up-regulated by quercetin.
"highlight2" >CBP↑,
"highlight2" >TSC2↑,
"highlight2" >HER2/EBBR2↓, erb-2
"highlight2" >BCR↓,
"highlight2" >TumCCA↑, quercetin significantly inhibited the expression of specific oncogenes and genes controlling G1, S, G2, and M phases of the cell cycle.
"highlight2" >chemoPv↑, Our results correlate with those of nutritional studies that support the roles of dietary bioflavonoids as cancer chemopreventive agents.

3338- QC,    Quercetin: Its Antioxidant Mechanism, Antibacterial Properties and Potential Application in Prevention and Control of Toxipathy
- Review, Var, NA - Review, Stroke, NA
"highlight2" >*antiOx↑, The antioxidant mechanism of quercetin in vivo is mainly reflected in its effects on glutathione (GSH), signal transduction pathways, reactive oxygen species (ROS), and enzyme activities.
"highlight2" >*GSH↑,
"highlight2" >*ROS↓,
"highlight2" >*Dose↑, antioxidant properties of quercetin show a concentration dependence in the low dose range but too much of the antioxidant brings about the opposite result
"highlight2" >*NADPH↓, quercetin counteracts atherosclerosis by reversing the increased expression of NADPH oxidase i
"highlight2" >*AMP↓, decreases in activation of AMP-activated protein kinase, thereby inhibiting NF-κB signaling
"highlight2" >*NF-kB↓,
"highlight2" >*p38↑, quercetin improves the antioxidant capacity of cells by activating the intracellular p38 MAPK pathway, increasing intracellular GSH levels and providing a source of hydrogen donors in the scavenging of free radical reactions.
"highlight2" >*MAPK↑,
"highlight2" >*SOD↑, quercetin achieves protection against acute spinal cord injury by up-regulating the activity of SOD, down-regulating the level of malondialdehyde (MDA), and inhibiting the p38MAPK/iNOS signaling pathway
"highlight2" >*MDA↓,
"highlight2" >*iNOS↓,
"highlight2" >*Catalase↑, quercetin reduces imiquimod (IMQ)-induced MDA levels in skin tissues and enhances catalase, SOD, and GSH activities, which together improve the antioxidant properties of the body
"highlight2" >*PI3K↑, It also controls the development of atherosclerosis induced by high fructose diet by enhancing PI3K/AKT and inhibiting ROS
"highlight2" >*Akt↑,
"highlight2" >*lipid-P↓, Quercetin enhances antioxidant activity and inhibits lipid cultivation, and it is effective in the treatment of oxidative liver damag
"highlight2" >*memory↑, reversed hypoxia-induced memory impairment
"highlight2" >*radioP↑, Quercetin protects cells from radiation and genotoxicity-induced damage by increasing endogenous antioxidant and scavenging free radical levels
"highlight2" >*neuroP↑, This suggests that quercetin may be a potential neuroprotective agent against ischemia, which protects CA1 vertebral neurons from I/R injury in the hippocampal region of animals
"highlight2" >*MDA↓, quercetin significantly reduced MDA levels and increased SOD and catalase levels.

1493- QC,    New quercetin-coated titanate nanotubes and their radiosensitization effect on human bladder cancer
- NA, Bladder, NA
"highlight2" >RadioS↑,
"highlight2" >ChemoSen↑,

3337- QC,    Endoplasmic Reticulum Stress-Relieving Effect of Quercetin in Thapsigargin-Treated Hepatocytes
- in-vitro, NA, HepG2
"highlight2" >*Inflam↓, quercetin exerts anti-inflammatory and anti–insulin resistance actions by suppressing UPR in cells experiencing ER stress
"highlight2" >*UPR↓,
"highlight2" >*GRP58↓, (GRP78) and the downstream proteins such as X-box binding protein 1 (XBP1). The increased expression was significantly inhibited by quercetin, indicating that this compound can relieve ER stress
"highlight2" >*XBP-1↓,
"highlight2" >*ER Stress↓, previous reports as well as our results, we suggest that quercetin can inhibit ER stress in hepatocytes
"highlight2" >*antiOx↑, Quercetin, a well-known antioxidant, is one of the most abundant flavonols in vegetables and fruits and has been shown to have many pharmacological actions
"highlight2" >TNF-α↓, Quercetin suppressed the increased expression of TNF-α significantly and dose-dependently
"highlight2" >p‑eIF2α↓, quercetin treatment suppressed the phosphorylation of eIF2α, IRE1α and JNK and the mRNA expression of XBP-1, GRP78 and CHOP
"highlight2" >p‑IRE1↓,
"highlight2" >p‑JNK↓,
"highlight2" >CHOP↓,

3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
"highlight2" >*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
"highlight2" >*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
"highlight2" >*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
"highlight2" >*Aβ↓,
"highlight2" >*Inflam↓,
"highlight2" >*BBB↝, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
"highlight2" >*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
"highlight2" >*iNOS↓,
"highlight2" >*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
"highlight2" >*cognitive↑,
"highlight2" >*AChE↓, Quercetin administration resulted in the inhibition of AChE
"highlight2" >*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
"highlight2" >*ROS↓,
"highlight2" >*ATP↑,
"highlight2" >*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
"highlight2" >*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
"highlight2" >*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation

3335- QC,    Recent advances on the improvement of quercetin bioavailability
- Review, NA, NA
"highlight2" >*BioAv↓, bioavailability of quercetin is relatively low (<10%)

3334- QC,    Pharmacokinetics of Quercetin Absorption from Apples and Onions in Healthy Humans
- Trial, Nor, NA
"highlight2" >*Half-Life↑, elimination half-time (t1/2 ) of females (93.8 h for AP and 15.2 h for OP) was much higher than that of males t1/2 of (29.9 h for AP and 13.4 h for OP).

2431- QC,    The Protective Effect of Quercetin against the Cytotoxicity Induced by Fumonisin B1 in Sertoli Cells
- in-vitro, Nor, TM4
"highlight2" >*Apoptosis↓, 40 μM quercetin improved cell viability, reduced apoptosis, and preserved cell functions.
"highlight2" >*ROS↓, Quercetin also decreased reactive oxygen species (ROS) levels in TM4 cells exposed to FB1
"highlight2" >*antiOx↓, enhanced the expression of antioxidant genes
"highlight2" >*MMP↑, improved mitochondrial membrane potential.
"highlight2" >*GPI↑, elevated the mRNA and protein expression of glycolysis-related genes, including (Gpi1), (Hk2), (Aldoa), (Pkm), lactate (Ldha) and (Pfkl)
"highlight2" >*HK2↑,
"highlight2" >*ALDOA↑,
"highlight2" >*PKM1↑,
"highlight2" >*LDHA↑,
"highlight2" >*PFKL↑,

2344- QC,    Quercetin: A natural solution with the potential to combat liver fibrosis
- Review, Nor, NA
"highlight2" >*HK2↓, By reducing the activity of key glycolytic enzymes—including hexokinase II (HK2), phosphofructokinase platelet (PFKP), and pyruvate kinase M2 (PKM2)—quercetin lowers energy production in LSECs, potentially slowing fibrosis progression.
"highlight2" >*PFKP↓,
"highlight2" >*PKM2↓,
"highlight2" >*hepatoP↑, Quercetin lowered levels of liver enzymes (ALT, AST) and total bile acid, markers of liver injury.
"highlight2" >*ALAT↓,
"highlight2" >*AST↓,
"highlight2" >*Glycolysis↓, quercetin inhibited glycolysis in LSECs, reducing lactate production, glucose consumption, and the expression of glycolytic enzymes
"highlight2" >*lactateProd↓,
"highlight2" >*GlucoseCon↓,
"highlight2" >*CXCL1↓, By suppressing CXCL1 secretion, quercetin decreased neutrophil infiltration, a key factor in liver fibrosis, thereby effecting inflammation control.
"highlight2" >*Inflam↓,

2343- QC,    Pharmacological Activity of Quercetin: An Updated Review
- Review, Nor, NA
"highlight2" >*ROS↓, Quercetin is a potent scavenger for ROS and hence protects the body against oxidative stress
"highlight2" >*GSH↑, Studies of animals and cells have shown that the synthesis of GSH is induced by quercetin.
"highlight2" >*Catalase↑, increased expression of superoxide dismutase (SOD), catalase (CAT), and GSH has been reported with the pretreatment of quercetin
"highlight2" >*SOD↑,
"highlight2" >*MDA↓, quercetin supplementation to layer chickens significantly reduced malondialdehyde (MDA) levels in the kidneys, liver, and heart and increased GSH, CAT, and glutathione peroxidase (GSH-Px) activities in the liver, kidney, and heart tissue
"highlight2" >*GPx↑,
"highlight2" >*Copper↓, In addition, quercetin can exert antioxidant effects by chelating Cu2+ and Fe2+ in its structure with catechol
"highlight2" >*Iron↓,
"highlight2" >Apoptosis↓, Quercetin inhibits the proliferation of liver cancer cells via induction of apoptosis and cell cycle arrest [43].
"highlight2" >TumCCA↑,
"highlight2" >MMP2↓, In HSC-6, SCC-9 human oral cancer cell lines, quercetin inhibits cell viability, migration, and invasion, reduces MMP-2 and MMP-9 abundance, downgrades miR-16, and upgrades HOXA10
"highlight2" >MMP9↓,
"highlight2" >GlucoseCon↓, quercetin inhibits the mobility of cancer cells by inhibiting glucose uptake and lactic acid production and reducing levels of PKM2, GLUT1, and LDHA, which may have a significant role in controlling breast cancer [56].
"highlight2" >lactateProd↓,
"highlight2" >PKM2↓,
"highlight2" >GLUT1↓,
"highlight2" >LDHA↓,
"highlight2" >ROS↑, Quercetin encapsulated in solid lipid nanoparticles ,MCF-7 and MCF-10A cells, Increase (ROS)

2342- QC,    Quercetin Inhibits the Proliferation of Glycolysis-Addicted HCC Cells by Reducing Hexokinase 2 and Akt-mTOR Pathway
- in-vitro, HCC, Bel-7402 - in-vitro, HCC, SMMC-7721 cell - in-vivo, NA, NA
"highlight2" >TumCP↓, In the present study, we reported that QUE inhibited the proliferation of HCC cells that relied on aerobic glycolysis.
"highlight2" >HK2↓, QUE could decrease the protein levels of HK2 and suppress the AKT/mTOR pathway in HCC cells
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >GlucoseCon↓, glucose uptake and lactate production of SMMC-7721 and Bel-7402 decreased in a dose-dependent manner after QUE treatment
"highlight2" >lactateProd↓,
"highlight2" >Glycolysis↓, QUE can inhibit the glycolysis of cancer cells, thereby inhibiting the progression of multiple cancers

2341- QC,    Quercetin suppresses the mobility of breast cancer by suppressing glycolysis through Akt-mTOR pathway mediated autophagy induction
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
"highlight2" >MMP2↓, quercetin treatment down-regulated the expression of cell migration marker proteins, such as matrix metalloproteinase 2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF).
"highlight2" >MMP9↓, level of MMP-2, MMP-9 and VEGF was all strongly cut down by quercetin treatment compared with control group
"highlight2" >VEGF↓,
"highlight2" >Glycolysis↓, quercetin successfully blocked cell glycolysis by inhibiting the level of glucose uptake and the production of lactic acid
"highlight2" >lactateProd↓,
"highlight2" >PKM2↓, and also decreased the level of glycolysis-related proteins Pyruvate kinase M2 (PKM2), Glucose transporter1(GLUT1) and Lactate dehydrogenase A (LDHA).
"highlight2" >GLUT1↓,
"highlight2" >LDHA↓,
"highlight2" >TumAuto↑, quercetin induced obvious autophagy via inactivating the Akt-mTOR pathway
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >TumMeta↓, Quercetin suppressed the progression of breast cancer by inhibiting tumor metastasis and glycolysis in vivo
"highlight2" >MMP3↓, quercetin effectively suppressed the invasion and migration ability of breast cancer cells through suppressing the expression of MMP-3, MMP-9 and VEGF,
"highlight2" >eff↓, down-regulating the expression of PKM2, which regulated the final step of glycolysis, could effectively enhance the chemotherapeutic effect of THP
"highlight2" >GlucoseCon↓, we found that quercetin effectively suppressed the level of glucose uptake and the production of lactic acid, and also down-regulated the expression of glycolysis-related proteins PKM2, LDHA and GLUT1,
"highlight2" >lactateProd↓,
"highlight2" >TumAuto↑, quercetin treatment induced obvious autophagy in MCF-7 and MDA-MB-231 cells via inactivating the Akt-mTOR pathway
"highlight2" >LC3B-II↑, showing obvious conversion of LC3B-I to LC3B-II

2340- QC,    Oral Squamous Cell Carcinoma Cells with Acquired Resistance to Erlotinib Are Sensitive to Anti-Cancer Effect of Quercetin via Pyruvate Kinase M2 (PKM2)
- in-vitro, OS, NA
"highlight2" >TumCG↓, At a concentration of 5 μM, quercetin effectively arrested cell growth, reduced glucose utilization, and inhibited cellular invasiveness
"highlight2" >GlucoseCon↓,
"highlight2" >TumCI↓,
"highlight2" >GLUT1↓, Quercetin also prominently down-regulated GLUT1, PKM2, and lactate dehydrogenase A (LDHA) expression of erlotinib-resistant HSC-3 cells
"highlight2" >PKM2↓,
"highlight2" >LDHA↓,
"highlight2" >Glycolysis↓, Moreover, quercetin (30 μM) suppressed glycolysis in the MCF-7 and MDA-MB-231 breast cancer cells, as evidenced by decreased glucose uptake and lactate production with a concomitant decrease in the levels of the GLUT1, PKM2, and LDHA proteins [29].
"highlight2" >lactateProd↓,
"highlight2" >HK2↓, Hexokinase 2 (HK2)-mediated glycolysis was also shown to be inhibited following quercetin treatment (25~50 μM) in Bel-7402 and SMMC-7721 hepatocellular carcinoma (HCC) cells
"highlight2" >eff↑, Downregulation of PKM2 also potently restored sensitivity to the inhibitory effect of erlotinib on cell growth and invasion

2339- QC,    Quercetin protects against LPS-induced lung injury in mice via SIRT1-mediated suppression of PKM2 nuclear accumulation
- in-vivo, Nor, NA
"highlight2" >*Inflam↓, Quercetin (Que) is a natural bioflavonoid compound with anti-inflammatory and antioxidative properties that reportedly inhibits the NLRP3 inflammasome in sepsis-induced organ dysfunctions such as ALI
"highlight2" >*antiOx↑,
"highlight2" >*NLRP3↓,
"highlight2" >*Sepsis↓,
"highlight2" >*PKM2↓, inhibit the activation of the NLRP3 inflammasome by suppressing the nuclear accumulation of PKM2 and increasing SIRT1 levels.
"highlight2" >*SIRT1↓,

2338- QC,    Quercetin: A Flavonoid with Potential for Treating Acute Lung Injury
- Review, Nor, NA
"highlight2" >*SIRT1↑, Quercetin increased SIRT1 expression in lung tissue, inhibited NLRP3 inflammasome activation, and reduced the release of pro-inflammatory factors (TNFα, IL-1β, and IL-6), preventing the up-regulation of nuclear PKM2 in the lung.
"highlight2" >*NLRP3↓,
"highlight2" >*Inflam↓,
"highlight2" >*TNF-α↓,
"highlight2" >*IL1β↓,
"highlight2" >*IL6↓,
"highlight2" >*PKM2↓, preventing the up-regulation of nuclear PKM2 in the lung.
"highlight2" >*HO-1↑, Quercetin increased HO-1 expression in the lungs of a septic lung injury mouse model
"highlight2" >*ROS↓, puncture in rats, showing that early administration of Quercetin reduced the levels of oxidative stress markers, such as xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA), and increased the levels of antioxidant enzymes in lung tiss
"highlight2" >*NO↓,
"highlight2" >*MDA↓,
"highlight2" >*antiOx↑,
"highlight2" >*COX2↓, Quercetin also reduced the expression of COX-2, HMGB1, and iNOS expression and NF-κB p65 phosphorylation
"highlight2" >*HMGB1↓,
"highlight2" >*iNOS↓,
"highlight2" >*NF-kB↓,

2303- QC,  doxoR,    Quercetin greatly improved therapeutic index of doxorubicin against 4T1 breast cancer by its opposing effects on HIF-1α in tumor and normal cells
- in-vitro, BC, 4T1 - in-vivo, NA, NA
"highlight2" >cardioP↑, Quercetin had better cardioprotective and hepatoprotective activities.
"highlight2" >hepatoP↑,
"highlight2" >TumCG↓, In vivo, quercetin suppressed tumor growth and prolonged survival in BALB/c mice bearing 4T1 breast cancer.
"highlight2" >OS↑,
"highlight2" >ChemoSen↑, quercetin enhanced therapeutic efficacy of DOX and simultaneously reduced DOX-induced toxic side effects
"highlight2" >chemoP↑, IC50 of DOX in combination with quercetin 10 or 25 uM was increased by three- and fourfold, respectively, compared with that of DOX alone
"highlight2" >Hif1a↓, Further study showed that quercetin suppressed intratumoral HIF-1α in a hypoxia-dependent way but increased its accumulation in normal cells
"highlight2" >*Hif1a↑,
"highlight2" >selectivity↑, quercetin could improve therapeutic index of DOX by its opposing effects on HIF-1α in tumor and normal cells
"highlight2" >TumVol↓,
"highlight2" >OS↑,

2300- QC,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
"highlight2" >AntiTum↑, Quercetin exerts promising anti-tumor effects via the regulation of various cancer signaling pathways
"highlight2" >Hif1a↓, Quercetin inhibited HIF-1 transcriptional activity in the HCT116 colon cancer cell line
"highlight2" >*Hif1a↑, On the contrary, quercetin increased the accumulation of HIF-1α in healthy cells
"highlight2" >Glycolysis↓, Quercetin inhibited glycolysis and proliferation of glycolysis-dependent hepatocellular carcinoma (SMMC-7721 and Bel-7402) cells by downregulating HKII;
"highlight2" >HK2↓,
"highlight2" >PDK3↓, quercetin inhibited PDK3 in hepatocellular carcinoma (HepG2) and lung cancer (A549) cells
"highlight2" >PFKP?, The ability of quercetin to impair PFKP-LDHA signaling

913- QC,    Effects of low dose quercetin: Cancer cell-specific inhibition of cell cycle progression
- in-vitro, BC, SkBr3 - in-vitro, BC, MDA-MB-435
"highlight2" >TumCP↓,
"highlight2" >TumCCA↑, arrest at the G1 phase
"highlight2" >DNAdam↑, mild DNA damage
"highlight2" >Chk2↑,
"highlight2" >CycB/CCNB1↓, cyclin B1
"highlight2" >CDK1↓,
"highlight2" >tumCV↓, 94% viability with 10uM
"highlight2" >p‑RB1↓, Rb
"highlight2" >P21↑,

1201- QC,    Quercetin: a silent retarder of fatty acid oxidation in breast cancer metastasis through steering of mitochondrial CPT1
- in-vivo, BC, NA
"highlight2" >mitResp↓, significant reduction in the intracellular mitochondrial respiration
"highlight2" >Glycolysis↓,
"highlight2" >ATP↓,
"highlight2" >ROS↑,
"highlight2" >GSH↓,
"highlight2" >TumMeta↓,
"highlight2" >Apoptosis↑,
"highlight2" >FAO↓,

980- QC,    Dietary Quercetin Exacerbates the Development of Estrogen-Induced Breast Tumors in Female ACI Rats
- in-vivo, BC, NA
"highlight2" >COMT↓, bad
"highlight2" >ROS∅, quercetin (2.5 g/kg food) does not confer protection against breast cancer, does not inhibit E2-induced oxidant stress and may exacerbate breast carcinogenesis in E2-treated ACI rats.

926- QC,  PacT,  doxoR,  Tam,    Bioenhancers from mother nature and their applicability in modern medicine
- Review, Nor, NA
"highlight2" >*BioEnh↑, Piperine, obtained from the oleoresin in the peppercorns is by far the most studied and researched bioenhancer.
"highlight2" >BioEnh↑, In a study, pretreatment of quercetin (5.0 and 15 mg/kg) half an hour before verapamil (10 mg/kg) administration significantly altered the pharmacokinetics of verapamil.
"highlight2" >BioEnh↑, genistein (10 mg/kg) caused an increase in AUC (54.7%) and a decrease in the total plasma clearance (35.2%) after oral administration of paclitaxel
"highlight2" >BioEnh↑, Oral naringin (3.3 and 10 mg/kg) was pretreated 30 min before and after intravenous administration of paclitaxel (3 mg/kg), the AUC was significantly improved (40.8% and 49.1% for naringin doses
"highlight2" >BioEnh↑, One of the widely used bioenhancers is Capmul MCM C10, a glyceryl monocaprate, produced from edible fats and oils and is commonly used in lip products.
"highlight2" >BioEnh↑, Nitrite glycoside is a bioenhancer for drugs and nutrients. Novel bioactive nitrile glycosides, niaziridin and niazirin is obtained from the leaves, pods, and bark of Moringa oleifera
"highlight2" >BioEnh↑, Cow urine distillate is more effective as bioenhancer than cow urine, to increase the effectiveness of antimicrobial, antifungal, and anticancer drugs.
"highlight2" >P-gp↓, Bioavailability-enhancing activity of natural compounds from the medicinal plants may be attributed to various mechanisms, such as P-gp inhibition activity by flavone, quercetin, and genistein

923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
"highlight2" >ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
"highlight2" >GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
"highlight2" >Ca+2↝,
"highlight2" >MMP↓,
"highlight2" >Casp3↑, activation of caspase-3, -8, and -9
"highlight2" >Casp8↑,
"highlight2" >Casp9↑,
"highlight2" >other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
"highlight2" >*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
"highlight2" >*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
"highlight2" >HO-1↑,
"highlight2" >TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
"highlight2" >Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
"highlight2" >STAT3↓,
"highlight2" >DR5↑, several studies showed that QC upregulated the death receptor (DR)
"highlight2" >P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
"highlight2" >MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
"highlight2" >IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
"highlight2" >IL6↓,
"highlight2" >COX2↓,
"highlight2" >IL8↓,
"highlight2" >iNOS↓,
"highlight2" >TNF-α↓,
"highlight2" >cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
"highlight2" >Apoptosis↑, increased apoptosis and p53 expression
"highlight2" >P53↑,
"highlight2" >Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
"highlight2" >survivin↓,
"highlight2" >TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
"highlight2" >Casp10↑,
"highlight2" >DFF45↑,
"highlight2" >TNFR 1↑,
"highlight2" >Fas↑,
"highlight2" >NF-kB↓,
"highlight2" >IKKα↓,
"highlight2" >cycD1/CCND1↓, SKOV3 Reduction in cyclin D1 level
"highlight2" >Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
"highlight2" >BAX↑,
"highlight2" >PI3K↓,
"highlight2" >Akt↓,
"highlight2" >E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
"highlight2" >Vim↓,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >cMyc↓,
"highlight2" >EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
"highlight2" >MMP2↓,
"highlight2" >NOTCH1↓,
"highlight2" >MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
"highlight2" >angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
"highlight2" >TSP-1↑,
"highlight2" >CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
"highlight2" >XIAP↓,
"highlight2" >Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
"highlight2" >Slug↓,
"highlight2" >LEF1↓,
"highlight2" >P-gp↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
"highlight2" >EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
"highlight2" >GSK‐3β↓,
"highlight2" >mTOR↓,
"highlight2" >RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
"highlight2" >HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
"highlight2" >VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
"highlight2" >TGF-β↓,
"highlight2" >COL1↓,
"highlight2" >COL3A1↓,

922- QC,    Quercetin and ovarian cancer: An evaluation based on a systematic review
- Review, NA, NA
"highlight2" >ROS↑, presence of peroxidases, Q reacts with H2O2 to form a Q-quinone (QQ) that has a pro-oxidant effect

921- QC,    Essential requirement of reduced glutathione (GSH) for the anti-oxidant effect of the flavonoid quercetin
- in-vitro, lymphoma, U937
"highlight2" >ROS↑, long periods it showed a pro-oxidant activity
"highlight2" >GSH↓, long periods

920- QC,    Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin
- Review, NA, NA
"highlight2" >GSH↓, Qu depletes GSH in a concentration-dependent manner;
"highlight2" >ROS↑, Because normal, non-transformed cells have a lower basal intracellular ROS level, and have a full antioxidant capacity, they should be less vulnerable to the ROS stress that is induced by Qu. ****

919- QC,    Quercetin Regulates Sestrin 2-AMPK-mTOR Signaling Pathway and Induces Apoptosis via Increased Intracellular ROS in HCT116 Colon Cancer Cells
- in-vitro, CRC, HCT116
"highlight2" >Apoptosis↑,
"highlight2" >ROS↑,
"highlight2" >SESN2↑,
"highlight2" >P53↑,
"highlight2" >AMPKα↑,
"highlight2" >mTOR↓,

918- QC,  CUR,  VitC,    Anti- and pro-oxidant effects of oxidized quercetin, curcumin or curcumin-related compounds with thiols or ascorbate as measured by the induction period method
- Analysis, NA, NA
"highlight2" >ROS↑, CUR enhances the prooxidant activity of ascorbate(vit C)
"highlight2" >ROS↑, Under anaerobic conditions, QUE, with a catechol ring, may be more prooxidant than CUR, with a phenol ring.

917- QC,  BML,  Pap,    Quercetin: A Versatile Flavonoid
- Review, Nor, NA
"highlight2" >*BioEnh↑, quercetin was combined with bromelain and papain, which may enhance its absorption and papain, which may enhance its absorption

916- QC,    Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells
- Review, Ovarian, NA
"highlight2" >COX2↓,
"highlight2" >CRP↓,
"highlight2" >ER Stress↑, Quercetin can result in stimulate the ER stress pathway that lead to the cause of cell death and apoptosis
"highlight2" >Apoptosis↑,
"highlight2" >GRP78/BiP↑,
"highlight2" >CHOP↑,
"highlight2" >p‑STAT3↓, quercetin suppresses STAT3 and PI3K/AKT/mTOR pathways
"highlight2" >PI3K↓,
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >cMyc↓, leading to downregulate the prosurvival cellular proteins expression, including cMyc, cyclin D1, and c-FLIP
"highlight2" >cycD1/CCND1↓,
"highlight2" >cFLIP↓,
"highlight2" >IL6↓, decreased the IL-6 and IL-10 release
"highlight2" >IL10↓,

915- QC,    Hormesis and synergy: pathways and mechanisms of quercetin in cancer prevention and management
- Review, NA, NA
"highlight2" >ROS↑, Pro-oxidant effects are present at cellular concentrations of 40–100uM

914- QC,    Quercetin and Cancer Chemoprevention
- Review, NA, NA
"highlight2" >GSH↓, high Qu concentration, causes a reduction in GSH content
"highlight2" >ROS↑, in tumor cells
"highlight2" >TumCCA↑, Depending on the cell type and tumor origin, Qu is able to block the cell cycle at G2/M or at the G1/S transition
"highlight2" >Ca+2↑, Qu treatment increases cytosolic Ca2+ levels
"highlight2" >MMP↓,
"highlight2" >Casp3↑,
"highlight2" >Casp8↑,
"highlight2" >Casp9↑,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >AMPKα↑,
"highlight2" >ASK1↑,
"highlight2" >p38↑,
"highlight2" >TRAIL↑, Qu is a potent enhancer of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, through the induction of the expression of death receptor (DR)-5, a phenomenon that specifically occurs in prostate cancer cells
"highlight2" >DR5↑,
"highlight2" >cFLIP↓,
"highlight2" >Apoptosis↑, tumor cell lines are prone to cell-cycle arrest and apoptosis at Qu concentrations that have no or little effect on non-transformed cells ****

60- QC,  EGCG,  isoFl,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, pCSCs
"highlight2" >Casp3↑, EGCG induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2, survivin and XIAP in CSCs.
"highlight2" >Casp7↑,
"highlight2" >Bcl-2↓,
"highlight2" >survivin↓,
"highlight2" >XIAP↓,
"highlight2" >EMT↓,
"highlight2" >Slug↓,
"highlight2" >Snail↓,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >LEF1↓, LEF-1/TCF
"highlight2" >CSCs↓, quercetin synergizes with EGCG in inhibiting the self-renewal properties of prostate CSCs, inducing apoptosis, and blocking CSC's migration and invasion.
"highlight2" >Apoptosis↑,
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,
"highlight2" >CD44↓, EGCG inhibits the self-renewal capacity of CD44+α2β1+CD133+ CSCs isolated from human primary prostate tumors,
"highlight2" >CD133↓,

52- QC,    Effect of Quercetin on Cell Cycle and Cyclin Expression in Ovarian Carcinoma and Osteosarcoma Cell Lines
- in-vitro, BC, MCF-7 - in-vitro, Ovarian, SKOV3 - in-vitro, OS, U2OS
"highlight2" >Bcl-2↓, quercetin treatment Bcl-2 expression decreased significantly while Bax expression increased significantly
"highlight2" >BAX↑,
"highlight2" >PI3K/Akt↓,
"highlight2" >cycD1/CCND1↓, The cyclin D1 expression was significantly decreased following the treatment with quercetin in SKOV3 and U2OSPt cells, but not in SKOV3/CDDP and U2OS cells
"highlight2" >TumCCA↑, quercetin influenced the G2/M phase of cell cycle, the flavonoid did not affect cyclin B1 levels in all cell lines, indicating the involvement of other possible mechanisms.

53- QC,    Quercetin regulates β-catenin signaling and reduces the migration of triple negative breast cancer
- in-vitro, BC, MDA-MB-231 - NA, NA, MDA-MB-468
"highlight2" >E-cadherin↑, quercetin can induce the expression of E-cadherin and also downregulate vimentin levels in TNBC
"highlight2" >Vim↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >cMyc↓,
"highlight2" >EMT↓, tumor cells
"highlight2" >TumCG↓, Quercetin Decreased the Growth and Cell Survival of TNBC Cells
"highlight2" >TumCMig↓, Quercetin Induced Change in Cell Morphology and Inhibited Cell Migration of TNBC Cell
"highlight2" >β-catenin/ZEB1↓, Quercetin Treatment Inactivated b-Catenin
"highlight2" >ChemoSen↑, Quercetin decreased the TGF-b1 signaling (Figure 6C) and also enhanced the ability of doxorubicin to decrease the migratory potential of TNBC.

54- QC,    Quercetin‑3‑methyl ether suppresses human breast cancer stem cell formation by inhibiting the Notch1 and PI3K/Akt signaling pathways
- in-vitro, BC, MCF-7
"highlight2" >EMT↓, led to the repression of EMT promotion
"highlight2" >E-cadherin↑,
"highlight2" >Vim↓,
"highlight2" >MMP2↓,
"highlight2" >NOTCH1↓, This agent also inhibited Notch1 and PI3K/Akt signalin
"highlight2" >PI3K/Akt↓,
"highlight2" >PI3k/Akt/mTOR↓,
"highlight2" >p‑Akt↓,
"highlight2" >EZH2↓, Querectin-3-methyl ether downregulates Notch1, PI3K-AKT and EZH2 signals in breast cancer cells
"highlight2" >H3K27ac↓, quercetin-3-methyl ether considerably decreased H3K27 methylation
"highlight2" >TumCCA↑, cell cycle dysregulation
"highlight2" >CSCs↓, which resulted in the downregulation of protein markers associated with cell cycle, apoptosis, stem cell pluripotency, and self-renewal, including CDK1, Cyclin B1, Bcl-xl, Bcl-2, Sox2 and Nanog
"highlight2" >CDK1↓,
"highlight2" >CycB/CCNB1↓,
"highlight2" >Bcl-xL↓,
"highlight2" >Bcl-2↓,
"highlight2" >Nanog↓,
"highlight2" >H3↓, Treatment with quercetin‑3‑methyl ether alone markedly suppressed the levels of tri‑methyl histone H3 (Lys27)

55- QC,    Quercetin inhibits the growth of human gastric cancer stem cells by inducing mitochondrial-dependent apoptosis through the inhibition of PI3K/Akt signaling
- in-vitro, GC, GCSCs
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >Cyt‑c↑, upregulation of Cyt-c following treatment with quercetin
"highlight2" >MMP↓, quercetin-induced apoptosis occurred via the mitochondrial-dependent pathway, which was mediated via the PI3K-Akt pathway.
"highlight2" >PI3K/Akt↓,
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >TumCG↓, quercetin has the potential to effectively intervene and prevent GCSC growth
"highlight2" >Apoptosis↑,
"highlight2" >CSCs↓, Quercetin inhibits the growth of human gastric cancer stem cells

56- QC,    Quercetin inhibits epithelial–mesenchymal transition, decreases invasiveness and metastasis, and reverses IL-6 induced epithelial–mesenchymal transition, expression of MMP by inhibiting STAT3 signaling in pancreatic cancer cells
- in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988
"highlight2" >EMT↓, quercetin inhibited EMT and decreased the secretion of matrix metalloproteinase (MMP).
"highlight2" >MMPs↓,
"highlight2" >MMP2↓,
"highlight2" >MMP7↓,
"highlight2" >STAT3↓, STAT3 phosphorylation decreased following treatment with quercetin.
"highlight2" >TumCI↓, quercetin can inhibit EMT, invasion, and metastasis and reverse the IL-6-induced increase in PC cell malignancy by inhibiting the STAT3 signaling pathway.
"highlight2" >TumMeta↓,
"highlight2" >tumCV↓, Quercetin decreases cell viability and inhibits EMT in PC cell lines

57- QC,    Quercetin inhibits angiogenesis through thrombospondin-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo
- vitro+vivo, PC, PC3
"highlight2" >TSP-1↑, protein + mRNA
"highlight2" >angioG↓, quercetin can effectively inhibit angiogenesis through TSP-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo.
"highlight2" >TumCMig↓, After treated with quercetin at 25, 50 and 100 µM for 24 h, the migration, invasion and tube formation were also inhibited
"highlight2" >TumCI↓,

58- QC,  doxoR,    Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin
- in-vitro, CRC, HT-29 - in-vitro, NA, CD133+
"highlight2" >Bcl-2↓,
"highlight2" >TumCCA↑, Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin
"highlight2" >CD133↓,
"highlight2" >CSCs↓,
"highlight2" >ChemoSen↑, adding quercetin to Dox chemotherapy is an effective strategy for treatment of both CSCs and bulk tumor cells.
"highlight2" >CycB/CCNB1↑, Quer induces G2/M phase accumulation due to enhanced level of the cyclin B and decreased level of the cyclin E, cyclin D, E2F1, and E2F2
"highlight2" >cycE/CCNE↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >E2Fs↓,

59- QC,    Quercetin Inhibits Breast Cancer Stem Cells via Downregulation of Aldehyde Dehydrogenase 1A1 (ALDH1A1), Chemokine Receptor Type 4 (CXCR4), Mucin 1 (MUC1), and Epithelial Cell Adhesion Molecule (EpCAM)
- in-vitro, BC, MDA-MB-231
"highlight2" >ALDH1A1↓, lowered the expression levels of proteins related to tumorigenesis and cancer progression, such as aldehyde dehydrogenase 1A1, C-X-C chemokine receptor type 4, mucin 1, and epithelial cell adhesion molecules.
"highlight2" >CXCR4↓,
"highlight2" >MUC1↓,
"highlight2" >EpCAM↓,
"highlight2" >CSCs↓, quercetin suppressed breast cancer stem cell proliferation, self-renewal, and invasiveness
"highlight2" >TumCP↓,
"highlight2" >TumCI↓,
"highlight2" >CD44↓, High doses of quercetin inhibit proliferation of MDA-MB-231 cells and CD44+/CD24− CSCs
"highlight2" >CD24↓,
"highlight2" >Apoptosis↑, Quercetin induces apoptosis of MDA-MB-231 cells
"highlight2" >TumCCA↑, These results indicate that quercetin alters the MDA-MB-231 cell cycle

51- QC,    Effect of Quercetin on Cell Cycle and Cyclin Expression in Ovarian Carcinoma and Osteosarcoma Cell Lines
- in-vitro, Ovarian, SKOV3
"highlight2" >cycD1/CCND1↓, The cyclin D1 expression was significantly decreased following the treatment with quercetin in SKOV3 and U2OSPt cells, but not in SKOV3/CDDP and U2OS cells
"highlight2" >TumCCA↑, quercetin influenced the G2/M phase of cell cycle

61- QC,    Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, ARPE-19
"highlight2" >p‑PI3K↓, combined therapy inhibited the phosphorylation of PI3K, AKT and ERK1/2, and reduced the protein expression of p38, ABCG2 and NF-κB.
"highlight2" >p‑Akt↓,
"highlight2" >p‑ERK↓,
"highlight2" >NF-kB↓,
"highlight2" >p38↓,
"highlight2" >ABCG2↓,
"highlight2" >CD44↓, Quercetin alone exhibited significant cytotoxic effects on CD44+/CD133+
"highlight2" >CD133↓,
"highlight2" >CSCs↓,

62- QC,  GoldNP,    Gold nanoparticles-conjugated quercetin induces apoptosis via inhibition of EGFR/PI3K/Akt-mediated pathway in breast cancer cell lines (MCF-7 and MDA-MB-231)
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
"highlight2" >EGFR↓, AuNPs-Qu-5 treatment inhibited the EGFR and its downstream signalling molecules PI3K/Akt/mTOR/GSK-3β.
"highlight2" >PI3k/Akt/mTOR↓, PI3K/Akt/mTOR/GSK-3β
"highlight2" >GSK‐3β↓,
"highlight2" >TumCP↓, AuNPs-Qu-5 in breast cancer cell lines curtails cell proliferation through induction of apoptosis and also suppresses EGFR signalling.
"highlight2" >Apoptosis↑,
"highlight2" >tumCV↓, Cell viability of free AuNPs, free Qu, and AuNPs‐Qu‐5 was tested on breast cancer cell lines (MCF‐7 and MDA‐MB‐231), and it was found that free Qu and AuNPs‐Qu‐5 decreased the cell viability.
"highlight2" >mTOR↓, AuNPs‐Qu‐5 treated cells downregulated mTOR protein and upregulated PTEN protein expression compared to free Qu
"highlight2" >PTEN↑,

63- QC,    Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells
- in-vitro, Pca, NA
"highlight2" >RAGE↓, Silencing RAGE expression by suppressing the PI3K/AKT/mTOR axis
"highlight2" >PI3K↓,
"highlight2" >mTOR↓,
"highlight2" >Akt↓,
"highlight2" >Apoptosis↑,
"highlight2" >TumAuto↑,
"highlight2" >ChemoSen↑, Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells

64- QC,    Quercetin enhances TRAIL-mediated apoptosis in colon cancer cells by inducing the accumulation of death receptors in lipid rafts
- in-vitro, Colon, HT-29 - in-vitro, Colon, SW-620 - in-vitro, Colon, Caco-2
"highlight2" >Cyt‑c↑, release of cytochrome c to the cytosol.
"highlight2" >BAX↑,
"highlight2" >Casp3↑,
"highlight2" >DR4↑, We report that quercetin enhanced TRAIL-induced apoptosis by causing the redistribution of DR4 and DR5 into lipid rafts.
"highlight2" >DR5↑,

65- QC,    Hsp27 participates in the maintenance of breast cancer stem cells through regulation of epithelial-mesenchymal transition and nuclear factor-κB
- in-vitro, BC, NA
"highlight2" >HSP27↓, Effectively suppressed the overexpression of Hsp27 and inhibit the breast cancer stem cells
"highlight2" >EMT↓, Knockdown of Hsp27 also suppressed EMT signatures, such as decreasing the expression of snail and vimentin and increasing the expression of E-cadherin.
"highlight2" >NF-kB↓,
"highlight2" >Snail↓,
"highlight2" >Vim↓,
"highlight2" >E-cadherin↑,
"highlight2" >CSCs↓, and inhibit the breast cancer stem cells

66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
"highlight2" >CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
"highlight2" >CDK1↓,
"highlight2" >EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
"highlight2" >PI3K↓, Inhibitory effects of quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
"highlight2" >MAPK↓,
"highlight2" >Wnt/(β-catenin)↓, wnt
"highlight2" >PSA↓,
"highlight2" >VEGF↓,
"highlight2" >PARP↑,
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >DR5↑,
"highlight2" >ROS⇅,
"highlight2" >Shh↓,
"highlight2" >P53↑, figure 1
"highlight2" >P21↑, quercetin regulates p21 expression
"highlight2" >EGFR↓,
"highlight2" >TumCCA↑, quercetin has cell-specific anti-proliferative impacts via stimulation of cell cycle arrest at the G1 stage.
"highlight2" >ROS↑, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
"highlight2" >miR-21↓,
"highlight2" >TumCP↓,
"highlight2" >selectivity↑, In breast cancer cells, quercetin inhibits cell proliferation without exerting any cytotoxic impact on normal breast epithelium
"highlight2" >PDGF↓, figure 1
"highlight2" >EGF↓,
"highlight2" >TNF-α↓,
"highlight2" >VEGFR2↓,
"highlight2" >mTOR↓,
"highlight2" >cMyc↓,
"highlight2" >MMPs↓,
"highlight2" >GRP78/BiP↑,
"highlight2" >CHOP↑,

67- QC,  RES,    Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
"highlight2" >cJun↑, Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
"highlight2" >AR↓,

98- QC,    Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway
- in-vivo, Stroke, NA
"highlight2" >*Bcl-2↑,
"highlight2" >*BAX↓,
"highlight2" >*Bax:Bcl2↓, Que postconditioning significantly decreased Bax expression and increased Bcl-2 expression
"highlight2" >*cardioP↑, cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.
"highlight2" >*Akt↑,
"highlight2" >*PI3K↑,
"highlight2" >*LDH↓, Que postconditioning reduced the levels of CK (1642.9±194.3 vs 2679.5±194.3 U/L, P<0.05) and LDH (1273.6±176.5 vs 2618±197.7 U/L, P<0.05) compared to the I/R group

43- QC,    Investigation of the anti-cancer effect of quercetin on HepG2 cells in vivo
- in-vivo, Liver, HepG3
"highlight2" >cycD1/CCND1↓, quercetin could significantly inhibit the growth and proliferation of HepG2 cells by regulating the gene expression of cyclin D1
"highlight2" >TumCG↓,
"highlight2" >TumCP↓,

35- QC,    Quercetin may act as a cytotoxic prooxidant after its metabolic activation to semiquinone and quinoidal product
- Study, NA, NA
"highlight2" >ROS↑, Quercetin may act as a cytotoxic prooxidant after its metabolic activation to semiquinone and quinoidal product
"highlight2" >GSH↓, depletion of GSH

36- QC,    Quercetin induces G2 phase arrest and apoptosis with the activation of p53 in an E6 expression-independent manner in HPV-positive human cervical cancer-derived cells
- in-vitro, Cerv, HeLa - in-vitro, Cerv, SiHa
"highlight2" >P53↑,
"highlight2" >P21↑,
"highlight2" >BAX↑,
"highlight2" >Casp3↑,
"highlight2" >Casp7↑,
"highlight2" >TumCCA↑, G2 phase arrest
"highlight2" >ROS↑, high concentrations (>40 µM) is able to act as a prooxidant
"highlight2" >TumCCA↑, Quercetin induces G2 phase arrest and apoptosis
"highlight2" >Apoptosis↑,

37- QC,    Low Concentrations of Flavonoids Are Protective in Rat H4IIE Cells Whereas High Concentrations Cause DNA Damage and Apoptosis
- in-vivo, Hepat, H4IIE
"highlight2" >DNAdamC↑,
"highlight2" >Casp1↑,
"highlight2" >BioAv↝, Published data on quercetin pharmacokinetics in humans suggest that a dietary supplement of 1–2 g of quercetin may result in plasma concentrations between 10 and 50 μmol/L

38- QC,    Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
"highlight2" >ROS⇅, LNCaP and PC-3 cells that have an oxidative cellular environment showed ROS quenching after quercetin treatment while DU-145 showed rise in ROS levels despite having a highly reductive environment.
"highlight2" >GSH↓,
"highlight2" >PI3K/Akt⇅, DU-145↓, PC3↑

39- QC,    A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells
- Analysis, NA, NA
"highlight2" >ROS↑, production of ROS in both cancer, and cancer stem cells,
"highlight2" >GSH↓, By directly reducing the intracellular pool of glutathione (GSH), QC can influence ROS metabolism
"highlight2" >IL6↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α, and many other cancer inflammatory mechanisms
"highlight2" >COX2↓,
"highlight2" >IL8↓,
"highlight2" >iNOS↓,
"highlight2" >TNF-α↓,
"highlight2" >MAPK↑, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
"highlight2" >ERK↑,
"highlight2" >SOD↑,
"highlight2" >ATP↓,
"highlight2" >Casp↑,
"highlight2" >PI3K/Akt↓,
"highlight2" >mTOR↓,
"highlight2" >NOTCH1↓,
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >IFN-γ↓,
"highlight2" >TumCP↓, QC directly involves inducing apoptosis and/or the cell cycle arrest process, and also inhibits the propagation of rapidly proliferating cells
"highlight2" >TumCCA↑,
"highlight2" >Akt↓, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
"highlight2" >P70S6K↓,
"highlight2" >*Keap1↓,
"highlight2" >*GPx↑, inhibiting its negative regulator, Keap1, resulting in Nrf-2 nuclear translocation [86]. This results in the production and activation of enzymes namely GPX, CAT, heme oxygenase 1 (HO-1), peroxiredoxin (PRX)
"highlight2" >*Catalase↑,
"highlight2" >*HO-1↑,
"highlight2" >*NRF2↑,
"highlight2" >NRF2↑, The effect of QC on nuclear translocation of Nrf-2 in a time-dependent manner, and increased expression level in HepG2, MgM (malignant mesothelioma) MSTO-211H, and H2452 cells at mRNA and protein quantity has been reported recently
"highlight2" >eff↑, quercetin coupled with gold nanoparticles promoted apoptosis by inhibiting the EGFR/P13K/Akt-mediated pathway
"highlight2" >HIF-1↓, Quercetin has been shown to suppress the Akt-mTOR pathway and hypoxia-induced factor 1 signaling pathway in gastric cancer cells, resulting in preventative autophagy

40- QC,    Quercetin arrests G2/M phase and induces caspase-dependent cell death in U937 cells
- in-vitro, lymphoma, U937
"highlight2" >cycD1/CCND1↓, dramatic changes in the level of cyclin B, cyclin D, and cyclin E
"highlight2" >cycE/CCNE↓,
"highlight2" >E2Fs↓,
"highlight2" >CycB/CCNB1↑, The G2/M phase accumulation was accompanied by an increase in the level of the cyclin B.
"highlight2" >Casp↑, These data clearly indicate that quercetin-induced apoptosis is associated with caspase activation
"highlight2" >Apoptosis↑,
"highlight2" >TumCCA↑, We report here that quercetin induces anti-proliferation and arrests G2/M phase in U937 cells.
"highlight2" >TumCP↓,

41- QC,    Quercetin induces mitochondrial-derived apoptosis via reactive oxygen species-mediated ERK activation in HL-60 leukemia cells and xenograft
- vitro+vivo, AML, HL-60
"highlight2" >Casp8↑, quercetin significantly induced caspase-8, caspase-9, and caspase-3 activation
"highlight2" >Casp9↑,
"highlight2" >Casp3↑,
"highlight2" >ROS↑, through induction of intracellular oxidative stress
"highlight2" >ERK↑, quercetin induced sustained activation of extracellular signal-regulated kinase (ERK)
"highlight2" >cl‑PARP↑, , poly ADP-ribose polymerase (PARP) cleavage, and mitochondrial membrane depolarization in HL-60 AML cells.
"highlight2" >MMP↓,
"highlight2" >eff↓, Moreover, both N-acetylcysteine(NAC) and the superoxide dismutase mimetic, MnTBAP, reversed quercetin-induced intracellular reactive oxygen species production, ERK activation, and subsequent cell death

42- QC,    Quercetin induces apoptosis by activating caspase-3 and regulating Bcl-2 and cyclooxygenase-2 pathways in human HL-60 cells
- in-vitro, AML, HL-60
"highlight2" >Bcl-2↓, x5.7, quercetin down-regulated the expression of anti-apoptosis protein Bcl-2 and up-regulated the expression of pro-apoptosis protein Bax.
"highlight2" >BAX↑, x2.9
"highlight2" >Casp3↑, x1.1, Caspase-3 was also activated by quercetin x1.1
"highlight2" >COX2↓, x1.4, quercetin inhibited the expression of the cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein.

68- QC,  BaP,    Differential protein expression of peroxiredoxin I and II by benzo(a)pyrene and quercetin treatment in 22Rv1 and PrEC prostate cell lines
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, PrEC
"highlight2" >PrxI∅, Prx-I, Prx-II PrEC cells
"highlight2" >PrxII∅, PrEC cells
"highlight2" >*toxicity↓, lack of quercetin-mediated changes in Prx expression suggests that quercetin does not interfere with H2O2 levels, and thus may have no deleterious effect in normal prostate cells
"highlight2" >ROS↓, <10uM Quercetin
"highlight2" >ROS↑, BaP-mediated toxicity in both 22Rv1 and PrEC cells was confirmed by a significant increase in reactive oxygen species
"highlight2" >ROS∅, Quercetin also antagonized the increase in ROS by BaP which suggests that BaP-mediated oxidative stress could be blocked with quercetin in 22Rv1 and PrEC cells. S
"highlight2" >chemoP↑, Studies have shown that quercetin can be a potential chemopreventative agent in prostate cancer.
"highlight2" >PrxII↑, A physiologically achievable concentration (5uM) of quercetin increased the expression of Prx II without affecting the Prx I levels in 22Rv1 cells
"highlight2" >i-H2O2↓, Upregulation of Prx II may reduce the intracellular levels of H 2 O2 which in turn can interfere with growth signaling pathways suppressing cell proliferation.

44- QC,    Preclinical Colorectal Cancer Chemopreventive Efficacy and p53-Modulating Activity of 3′,4′,5′-Trimethoxyflavonol, a Quercetin Analog
- in-vivo, CRC, HCT116
"highlight2" >P53↑, p53 expression was increased, 3-fold in ApcMin and 1.5-fold in HCT116 tumor-bearing mice
"highlight2" >chemoPv↑, Chemopreventive Efficacy
"highlight2" >TumVol↓, The TMFol early regimen approximately halved HCT116 tumor size
"highlight2" >TumCP↓, decreased tumor proliferation and increased apoptosi
"highlight2" >Apoptosis↑,

45- QC,    Quercetin Inhibit Human SW480 Colon Cancer Growth in Association with Inhibition of Cyclin D1 and Survivin Expression through Wnt/β-Catenin Signaling Pathway
- in-vitro, Colon, CX-1 - in-vitro, Colon, SW480 - in-vitro, Colon, HT-29 - in-vitro, Colon, HCT116
"highlight2" >cycD1/CCND1↓, Cyclin D(1) and the survivin gene were downregulated markedly by quercetin in a dose-dependent manner
"highlight2" >survivin↓,
"highlight2" >Wnt/(β-catenin)↓, Quercetin downregulated transcriptional activity of beta-catenin/Tcf in SW480 cells transiently transfected with the TCF-4 reporter gene.
"highlight2" >tumCV↓, Quercetin reduced cell viability in a dose- and time-dependent manner in SW480 and clone 26 cells
"highlight2" >TumCCA↑, The percentages of SW480 cells and clone 26 cells at G(2)/M phase were increased significantly after treatment with 40 approximately 80 micromol/L quercetin for 48 hours.
"highlight2" >Apoptosis↑, Quercetin induced the apoptosis of SW480 cells in a dose-dependent manner at the concentration of 20, 40, 60, anf 80 micromol/L.

46- QC,    Quercetin, but Not Its Glycosidated Conjugate Rutin, Inhibits Azoxymethane-Induced Colorectal Carcinogenesis in F344 Rats
- in-vitro, Colon, F344
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >BioAv↓, The lack of protection by rutin is probably due to its low bioavailability.

47- QC,    Induction of death receptor 5 and suppression of survivin contribute to sensitization of TRAIL-induced cytotoxicity by quercetin in non-small cell lung cancer cells
- in-vitro, NSCLC, H460 - in-vitro, NSCLC, A549
"highlight2" >TRAIL↑, quercetin sensitizes TRAIL-induced cytotoxicity in lung cancer cells
"highlight2" >DR5↑, induction of DR5 and suppression of survivin expression
"highlight2" >survivin↓,

48- QC,    Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells
- in-vitro, NSCLC, H460
"highlight2" >TRAILR↑, quercetin increased the expression of genes associated with death receptor signaling tumor necrosis factor-related apoptosis-inducing ligand receptor (TRAILR), caspase-10, interleukin (IL) 1R DNA fragmentation faotor 45 (DFF45), tumor necrosis fact
"highlight2" >Casp10↑,
"highlight2" >DFF45↑,
"highlight2" >TNFR 1↑,
"highlight2" >Fas↑,
"highlight2" >NF-kB↓, Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells
"highlight2" >IKKα↓,

49- QC,    Plasma rich in quercetin metabolites induces G2/M arrest by upregulating PPAR-γ expression in human A549 lung cancer cells
- in-vitro, Lung, A549
"highlight2" >CDK1↓, significantly suppressed the effects of 10 % QMP on cell proliferation and on the expression of cyclin B and cdk1. T
"highlight2" >CycB/CCNB1↓,
"highlight2" >PPARγ↑, activation of PPAR- γ plays an important role, at least in part, in the antiproliferative effects of quercetin metabolites.

50- QC,    Anticancer effect and mechanism of polymer micelle-encapsulated quercetin on ovarian cancer
- vitro+vivo, Ovarian, A2780S
"highlight2" >Casp3↑, Quercetin treatment induced the apoptosis of A2780S cells associated with activating caspase-3 and caspase-9.
"highlight2" >Casp9↑,
"highlight2" >Mcl-1↓, MCL-1 downregulation, Bcl-2 downregulation, Bax upregulation and mitochondrial transmembrane potential change were observed
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >angioG↓, inhibiting angiogenesis in vivo.
"highlight2" >TumCG↓, QU inhibited the growth of A2780S ovarian cancer cells on a dose dependent manner in vitro
"highlight2" >Apoptosis↑, quercetin may induce apoptosis of A2780S cells through the mitochondrial apoptotic pathway
"highlight2" >p‑p44↓, quercetin treatment decreased phosphorylated p44/42 mitogen-activated protein kinase and phosphorylated Akt, contributing to inhibition of A2780S cell proliferation.
"highlight2" >Akt↓,
"highlight2" >TumCP↓,
"highlight2" >eff↑, Our data suggested that QU/MPEG-PCL micelles were a novel nano-formulation of quercetin with a potential clinical application in ovarian cancer therapy.

86- QC,  PacT,    Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3)
- vitro+vivo, Pca, PC3
"highlight2" >BAD↑, Quercetin up regulate mRNA and protein levels of Bad
"highlight2" >IGFBP3↑,
"highlight2" >Cyt‑c↑, Quercetin significantly increases the proapoptotic mRNA levels of Bad, IGFBP-3 and protein levels of Bad, cytochrome C, cleaved caspase-9, caspase-10, cleaved PARP and caspase-3 activity in PC-3 cells
"highlight2" >cl‑Casp9↑, cleaved
"highlight2" >Casp10↑,
"highlight2" >cl‑PARP↑, Quercetin increases protein expression of cytochrome C and PARP
"highlight2" >Casp3↑,
"highlight2" >IGF-1R↓,
"highlight2" >PI3K↓, PI3K expression significantly decreased after quercetin treatment
"highlight2" >p‑Akt↓,
"highlight2" >cycD1/CCND1↓, protein
"highlight2" >IGF-1↓, mRNA levels of IGF-1,IGR-2, IGF-1R
"highlight2" >IGF-2↓,
"highlight2" >IGF-1R↓,
"highlight2" >MMP↓, Apoptosis is confirmed by loss of mitochondrial membrane potential in quercetin treated PC-3 cells.
"highlight2" >Apoptosis↑, uercetin treatment has been associated with antiproliferative effects [39] and induction of apop- tosis in cancer cells but not in normal cells [40].
"highlight2" >NA?,

97- QC,  HPT,    Effects of the flavonoid drug Quercetin on the response of human prostate tumours to hyperthermia in vitro and in vivo
- in-vitro, Pca, PC3
"highlight2" >HSP72↑, Quercetin in prostate cancer treatment is that it antagonizes HSP72 production and, thus, sensi- tizes cells to hyperthermia-induce d apoptosis
"highlight2" >TumCG↓, Quercetin dose-dependently suppressed PC-3 tumour growth in vitro and in vivo.
"highlight2" >eff↑, suggest the use of Quercetin as a hyperthermia sensitizer in the treatment of prostate carcinoma
"highlight2" >ChemoSen↑, Quercetin can act as a sensitizer to hyperthermia (® gures 1± 5), chemotherapeutic agents and ionizing radiation4,20
"highlight2" >RadioS↑,

96- QC,  docx,    Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/Akt signaling pathways
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
"highlight2" >PI3K/Akt↓, PI3K/Akt signaling pathway was excessively activated after prostate cancer cells developed resistance to docetaxel. And quercetin could also reverse the activation of this pathway.
"highlight2" >Ki-67↓,
"highlight2" >BAX↑,
"highlight2" >Bcl-2↓,
"highlight2" >EpCAM↓,
"highlight2" >Twist↓, Twist2
"highlight2" >E-cadherin↑,
"highlight2" >P-gp↓, Quercetin reverses docetaxel resistance by reversing the up-regulation of P-gp
"highlight2" >TumCP↓, quercetin had the reversal effect of docetaxel-resistance, which could inhibit cell proliferation, migration, invasion and colony formation of docetaxel-resistant prostate cancer cells.
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,

95- QC,    Quercetin, a natural dietary flavonoid, acts as a chemopreventive agent
- in-vitro, Pca, PC3
"highlight2" >p‑ERK↓, ERK1/2
"highlight2" >p‑STAT3↓, pSTAT3
"highlight2" >p‑Akt↓,
"highlight2" >N-cadherin↓,
"highlight2" >Vim↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >Snail↓,
"highlight2" >Slug↓,
"highlight2" >Twist↓, mRNA
"highlight2" >PCNA↓, simultaneous quercetin supplementation significantly decreased PCNA, N-cadherin, vimentin, and cyclin D1 protein levels compared to chemically induced cancer rats.
"highlight2" >EGFR↓, by inhibiting the EGFR signaling pathway and by regulating cell adhesion molecules in Sprague Dawley rats.
"highlight2" >chemoPv↑, acts as a chemopreventive agent

94- QC,  HPT,    Effects of quercetin on the heat-induced cytotoxicity of prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, Pca, JCA-1
"highlight2" >HSP70/HSPA5↓, Quercetin inhibited an increase of hsp70 expression after heat treatment and increased the number of subG1 cells with lower levels of hsp70 in JCA-1 and LNcap cells.
"highlight2" >TumCCA↑,
"highlight2" >TumCG↓, Quercetin inhibited the growth of JCA-1 and LNcap cells at concentrations over 12.5 mmol/L.
"highlight2" >eff↑, the presence of quercetin during heating enhances the growth-inhibitory effect of heat by inducing apoptosis in the JCA-1 and LNcap cells.

93- QC,    Chemical Proteomics Identifies Heterogeneous Nuclear Ribonucleoprotein (hnRNP) A1 as the Molecular Target of Quercetin in Its Anti-cancer Effects in PC-3 Cells
- in-vitro, Pca, PC3
"highlight2" >hnRNPA1↓, We found that quercetin bound the C-terminal region of hnRNPA1, impairing the ability of hnRNPA1 to shuttle between the nucleus and cytoplasm and ultimately resulting in its cytoplasmic retention.
"highlight2" >Casp3↑, activated caspase-3/7
"highlight2" >Casp7↑,
"highlight2" >TumCD↑, quercetin induced cell death in a time- and concentration-dependent manner.
"highlight2" >IAP1↓, We found quercetin mediated cytoplasmic accumulation of hnRNPA1, resulting in decreased cIAP1 protein levels.

92- QC,    Quercetin Inhibits Angiogenesis Mediated Human Prostate Tumor Growth by Targeting VEGFR- 2 Regulated AKT/mTOR/P70S6K Signaling Pathways
- vitro+vivo, Pca, HUVECs - vitro+vivo, Pca, PC3
"highlight2" >VEGFR2↓, Quercetin treatment inhibited the activation of VEGF-R2 and thereby suppressed the AKT/mTOR/P70S6K mediated angiogenesis signaling pathways.
"highlight2" >HemoG↓,
"highlight2" >Akt↓, AKT/mTOR/P70S6K↓
"highlight2" >mTOR↓,
"highlight2" >P70S6K↓,
"highlight2" >angioG↓, quercetin is a potent inhibitor of angiogenesis in vitro, ex vivo and in vivo.

91- QC,    The roles of endoplasmic reticulum stress and mitochondrial apoptotic signaling pathway in quercetin-mediated cell death of human prostate cancer PC-3 cells
- in-vitro, Pca, PC3
"highlight2" >CDK2↓, decreasing the levels of CDK2, cyclins E, and D proteins
"highlight2" >cycE/CCNE↓,
"highlight2" >cycD1/CCND1↓, proteins
"highlight2" >ATFs↑, Quercetin also stimulated the protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress
"highlight2" >GRP78/BiP↑,
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑, quercetin may induce apoptosis by direct activation of caspase cascade through mitochondrial pathway and ER stress in PC-3 cells.
"highlight2" >Casp3↑, Quercetin Promoted the Activations of Caspase-3, -8, and -9 in PC-3 Cells
"highlight2" >Casp8↑,
"highlight2" >Casp9↑,
"highlight2" >ER Stress↑, stress
"highlight2" >CHOP↑,
"highlight2" >TumCCA↑, quercetin at 150 μM caused G0/G1 phase arrest (31.4-49.7%) and sub-G1 phase cells (19.77%) for 36 h treatment and this effect is a time-dependent manner.
"highlight2" >DNAdam↑, incubation with quercetin for 48 h showed an apoptotic cell death and DNA damage
"highlight2" >AIF↑, quercetin promoted the trafficking of AIF protein released from mitochondria to nuclei.
"highlight2" >Ca+2↑, quercetin-treated PC-3 cells led to the significant changes in Ca 21 concentrations of PC-3 cells from 3 h and up to 12 h [Fig. 4
"highlight2" >MMP↓, quercetin significantly decreased the levels of DCm in PC-3 cells in a time-dependent course

90- QC,  HP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
"highlight2" >ROS↑, QH decreased the production of reactive oxygen species (ROS) and increased antioxidant capacity in PC3 cells at various concentrations (2.5‑60 µg/ml) with peak inhibition and augmentation changes of 3.22‑ and 3.00‑fold, respectively.
"highlight2" >cl‑Casp3↑, activated/cleaved caspase-3 levels were found to be elevated at low concentration of QH (5 and 10 μg/ml) by ~1.5-fold and at higher concentrations (20 and 40 μg/ml) by ~2.7-fold (Fig. 2E). Poly(adenosine diphosphate ribose)
"highlight2" >cl‑PARP↑, analysis revealed an increase in PARP cleavage in PC3 cells following QH treatment
"highlight2" >miR-21↓, dose-dependent decrease in miR-21 expression, with inhibition rates of 42, 56 and 77% observed at 5, 10 and 20 μg/ml QH, respectively
"highlight2" >PDCD4↑,
"highlight2" >TAC↑,
"highlight2" >tumCV↓, QH inhibits PC3 cell viability.
"highlight2" >TumCI↓, QH inhibits the invasive activity of PC3 cells.

89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
"highlight2" >PI3K/Akt↓, quercetin targeted c-met to inhibit the PI3K/AKT pathway in doxorubicin-resistant prostate cancer cells.
"highlight2" >cMET↓, quercetin treatment significantly inhibited c-met expression in PC3/R cells
"highlight2" >Casp3↑, combination treatment with quercetin to induce expression of cleaved caspase-3 and −9
"highlight2" >Casp9↑,
"highlight2" >MMP↓, combination treatment with quercetin and doxorubicin induced a significant decrease of MMP in PC3/R cells compared with cells treated with doxorubicin alone.
"highlight2" >ChemoSen↑, Quercetin increased the sensitivity of PC3/R cells to doxorubicin
"highlight2" >ROS↑, ROS, which are considered to be key apoptotic inducers (17) were released from the mitochondria into the cytoplasm, due to MMP collapse induced by co-treatment with quercetin and doxorubicin

88- QC,  PacT,    Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production
- vitro+vivo, Pca, PC3
"highlight2" >ROS↑, quercetin and paclitaxel significantly inhibited cell proliferation, increased apoptosis, arrested the cell cycle at the G2/M phase, inhibited cell migration, dramatically induced ER stress to occur, and increased ROS generation.
"highlight2" >ER Stress↑,
"highlight2" >TumCP↓,
"highlight2" >Apoptosis↑,
"highlight2" >TumCCA↑,
"highlight2" >TumCMig↓,
"highlight2" >GRP78/BiP↑, The combined group effectively decreased hnRNPA1 gene expressions and increased the GRP78 and CHOP gene expressions, which are related to ER stress and ROS production
"highlight2" >CHOP↑,
"highlight2" >TumCG↓, In vivo Tumor Growth Inhibition

87- QC,    Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
"highlight2" >ROS⇅,
"highlight2" >BAX↑, quercetin treatment increased BAX levels
"highlight2" >PUMA⇅,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >Shc↓,
"highlight2" >TAp63α↑, DU-145
"highlight2" >MAPK↑, DU-145 DU-145
"highlight2" >p‑p42↑,
"highlight2" >p‑p44↑,
"highlight2" >BIM↑, . In androgen-independent PCa cells with mutated p53 (DU-145), quercetin treatment increases cellular BAX levels whereas PUMA and BIM increased

69- QC,    Quercetin enhances TRAIL-induced apoptosis in prostate cancer cells via increased protein stability of death receptor 5
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
"highlight2" >TRAIL↑, Quercetin treatment enhanced TRAIL-induced activation proteins in the caspase pathway, such as poly (ADP-ribose) polymerase (PARP), caspase-3, and caspase-9.
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >Casp8↑,
"highlight2" >DR5↑, quercetin increases the stability of the DR5 protein, which results in synergistic enhancement of TRAIL-induced apoptosis in human prostate cancer cells.

85- QC,    Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC-3)
- in-vitro, Pca, PC3
"highlight2" >uPA↓, Quercetin downregulates uPA, uPAR and EGF, EGF-R mRNA expressions.
"highlight2" >uPAR↓,
"highlight2" >EGFR↓,
"highlight2" >NRAS↓,
"highlight2" >Jun↓,
"highlight2" >NF-kB↓, Quercetin inhibits cell survival factor β-catenin, NF-κB and also proliferative signalling molecules such as p-EGF-R, N-Ras, Raf-1, c.Fos c.Jun and p-c.Jun protein expressions
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >p38↑,
"highlight2" >MAPK↑,
"highlight2" >cJun↓,
"highlight2" >cFos↓,
"highlight2" >Raf↓, Raf-1
"highlight2" >TumCI↓, PC-3 cells are treated with quercetin, which inhibits invasion and migration of PC-3 cells.
"highlight2" >TumCMig↓,

84- QC,    Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression
- in-vitro, Pca, PC3
"highlight2" >P21↑, Addition of quercetin led to substantial decrease in the expression of Cdc2/Cdk-1, cyclin B1 and phosphorylated pRb and increase in p21.
"highlight2" >cDC2↓, Cdc2/Cdk-1
"highlight2" >CDK1↓, Cdc2/Cdk-1
"highlight2" >CycB/CCNB1↓,
"highlight2" >Casp3↑,
"highlight2" >Bcl-2↓,
"highlight2" >Bcl-xL↓, Apoptosis markers like Bcl-2 and Bcl-X(L) were significantly decreased and Bax and caspase-3 were increased.
"highlight2" >BAX↑,
"highlight2" >pRB↓,
"highlight2" >TumCCA↑, Flowcytometric analysis showed that quercetin blocks G2-M transition, with significant induction of apoptosis.
"highlight2" >Apoptosis↑,

74- QC,  EGCG,    Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancer
- Human, Pca, NA
"highlight2" >BioAv↑, We evaluated if chronic consumption of quercetin (Q) with green tea extract (GTE) enhances the bioavailability of GT polyphenols (GTPs) and reduces methylation activity as previously observed in mouse xenograft tumors.
"highlight2" >BioAv↑, Q was increased 14-fold, 12-fold and 4.5-fold in plasma, urine, and prostate tissue, respectively, in the GT + Q compared to the GT + PL-group.
"highlight2" >toxicity↓, No liver toxicity was observed.

70- QC,    Quercetin inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
"highlight2" >PSA↓, quercetin inhibited the secretion of the prostate-specific, androgen-regulated tumor markers, PSA and hK2
"highlight2" >AR↓, Quercetin inhibits the expression of AR protein
"highlight2" >NKX3.1↓, Quercetin can also significantly down-regulate the expression of another prostate-specific gene, NKX3.1,
"highlight2" >HK2↓, Quercetin inhibits PSA and hK2 secretion

71- QC,    Role of Bax in quercetin-induced apoptosis in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PrEC - in-vitro, Pca, YPEN-1 - in-vitro, Pca, HCT116
"highlight2" >Casp8↑, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
"highlight2" >Casp9↑,
"highlight2" >PARP↑,
"highlight2" >BAD↓,
"highlight2" >BAX↑,
"highlight2" >PI3K/Akt↓, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
"highlight2" >Cyt‑c↑, accompanied by cytochrome c release, and procaspases-3, -8 and -9 cleavage and increased poly (ADP-ribose) polymerase (PARP) cleavage.
"highlight2" >selectivity↑, quercetin treatment did not affect the viability or rate of apoptosis in normal human prostate epithelial cell line (PrEC)

72- QC,  Se,    Selenium- or quercetin-induced retardation of DNA synthesis in primary prostate cells occurs in the presence of a concomitant reduction in androgen-receptor activity
- in-vitro, Pca, PECs - in-vitro, Pca, LNCaP - in-vitro, Pca, NIH-3T3
"highlight2" >AR↓, In LNCaP cells transfected with an androgen-receptor (AR)-reporter gene coupled to luciferase, selenomethionine or quercetin reduced AR activity

73- QC,    The dietary bioflavonoid, quercetin, selectively induces apoptosis of prostate cancer cells by down-regulating the expression of heat shock protein 90
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
"highlight2" >HSP90↓, quercetin down-regulates the expression of Hsp90 which, in turn, induces inhibition of growth and cell death in prostate cancer cells
"highlight2" >Casp3↑, quercetin increased caspase-3 and caspase-9 activities in both LNCaP and PC-3 cells, whereas dihydroquercetin had no effect on caspases
"highlight2" >Casp9↑,
"highlight2" >TumCG↓,
"highlight2" >TumCD↑,
"highlight2" >selectivity↑, while exerting no quantifiable effect on normal prostate epithelial cells.
"highlight2" >toxicity↓, quercetin at doses of 40–1,900 mg/kg/day in rats showed no signs of toxicity or death

75- QC,  ENZ,    Quercetin targets hnRNPA1 to overcome enzalutamide resistance in prostate cancer cells
- in-vitro, Pca, HEK293 - in-vitro, NA, 22Rv1 - in-vitro, NA, C4-2B
"highlight2" >hnRNPA1↓, quercetin downregulates hnRNPA1 expression
"highlight2" >PSA↓,
"highlight2" >NKX3.1↓,
"highlight2" >FKBP5↓,
"highlight2" >UBE2C↓,
"highlight2" >AR-FL↓, FL AR
"highlight2" >AR-V7↑, downregulates the expression of AR-V7, antagonizes androgen receptor signaling
"highlight2" >AR↓, Quercetin downregulates androgen receptor signaling
"highlight2" >eff↑, Quercetin resensitizes enzalutamide-resistant xenografts to enzalutamide in vivo
"highlight2" >TumVol↓,
"highlight2" >BioAv↓, The bioavailability of quercetin is low as it is present in glycosylated form, which can be readily metabolized by enzymes in the gut and liver, leading to low systemic concentrations in the body

76- QC,    Multifaceted preventive effects of single agent quercetin on a human prostate adenocarcinoma cell line (PC-3): implications for nutritional transcriptomics and multi-target therapy
- in-vitro, Pca, PC3
"highlight2" >aSmase↝, Figure 3b shows that quercetin treatment caused a dose-dependent augmentation in mRNA levels of Diablo and FAS
"highlight2" >Diablo↑,
"highlight2" >Fas↓,
"highlight2" >Hsc70↓, coupled with a dose-responsive reduction in transcriptional activity of HSC70, HIF1A, Mcl-1, Hsp90 and BIRC4.
"highlight2" >Hif1a↓,
"highlight2" >Mcl-1↓,
"highlight2" >HSP90↓,
"highlight2" >FLT4↓, A dose-dependent drop in mRNA levels of FLT4, EPHB4, DNAPK, PARP1, ATM, perlecan, GnTV and heparanase genes was observed after treatment of PC-3 cells with quercetin
"highlight2" >EphB4↓,
"highlight2" >DNA-PK↓,
"highlight2" >PARP1↓,
"highlight2" >ATM↓,
"highlight2" >XIAP↝,
"highlight2" >PLC↓,
"highlight2" >GnT-V↝,
"highlight2" >heparanase↝,
"highlight2" >NM23↑, quercetin significantly exerted a dose-responsive rise in transcriptional levels of NM23 and CSR1 genes
"highlight2" >CSR1↑,
"highlight2" >SPP1↓, coupled with an expressive lowering in mRNA levels of SPP1, DNMT1, HDAC4, CXCR4, b-catenin and NHE1.
"highlight2" >DNMT1↓,
"highlight2" >HDAC4↓,
"highlight2" >CXCR4↓,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >FBXW7↝,
"highlight2" >AMACR↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >IGF-1R↓, down-regulation of mRNA levels of AMACR, cyclin D1, NOS2A, IGF1R, IMPDH1, IMPDH2 and HEC1
"highlight2" >IMPDH1↓,
"highlight2" >IMPDH2↓,
"highlight2" >HEC1↓,
"highlight2" >NHE1↓,
"highlight2" >NOS2↓,

77- QC,  EGCG,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, CD44+ - in-vitro, NA, CD133+ - in-vitro, NA, PC3 - in-vitro, NA, LNCaP
"highlight2" >Casp3↑, EGCG induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2, survivin and XIAP in CSCs.
"highlight2" >Casp7↑,
"highlight2" >Bcl-2↓,
"highlight2" >survivin↓,
"highlight2" >XIAP↓,
"highlight2" >EMT↓, EGCG inhibits epithelial-mesenchymal transition by inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF
"highlight2" >Vim↓,
"highlight2" >Slug↓,
"highlight2" >Snail↓,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >LEF1↓, LEF1/TCF
"highlight2" >TCF↓, LEF1/TCF
"highlight2" >eff↑, inhibition of Nanog by shRNA enhanced the inhibitory effects of EGCG
"highlight2" >CSCs↓, prostate cancer cell lines contain a small population of CD44+CD133+ cancer stem cells and their self-renewal capacity is inhibited by EGCG.
"highlight2" >TumCG↓, EGCG inhibits the growth of cancer stem cells isolated from human prostate cancer cell lines
"highlight2" >tumCV↓, EGCG inhibits the formation of primary and secondary tumor spheroids and cell viability of human prostate cancer stem cells

78- QC,    Effects of quercetin on insulin-like growth factors (IGFs) and their binding protein-3 (IGFBP-3) secretion and induction of apoptosis in human prostate cancer cells
- in-vitro, Pca, PC3
"highlight2" >IGF-1↓, and significantly reduced the both IGF-I and IGF-II levels.
"highlight2" >IGF-2↓,
"highlight2" >IGFBP3↑, At a dose of 100 μM concentration, we observed increased IGFBP-3 accumulation in PC-3 cells
"highlight2" >Bcl-2↓, Bcl-2 and Bcl-xL protein expressions were significantly decreased and Bax and caspase-3 were increased.
"highlight2" >Bcl-xL↓,
"highlight2" >Casp3↑,
"highlight2" >Apoptosis↑, Apoptosis induction was also confirmed by TUNEL assay.
"highlight2" >BAX↑,
"highlight2" >DNAdam↑, quercetin treated cells showed quercetin treatment caused DNA fragmentation in the PC-3 cells

79- QC,    Chemopreventive Effect of Quercetin in MNU and Testosterone Induced Prostate Cancer of Sprague-Dawley Rats
- in-vivo, Pca, NA
"highlight2" >GSH↑, The lipid peroxidation, H2O2, in (MNU+T) treated rats were increased and GSH level was decreased, whereas simultaneous quercetin-treated rats reverted back to normal level
"highlight2" >SOD↑,
"highlight2" >Catalase↑,
"highlight2" >GPx↑, SOD, catalase, GPX, Glutathionereductase, GST activities were significantly decreased in VP & DLP ofcancer-induced rats compared to control. Whereas, simultaneousquercetin supplement showed increased activities. (PDF) Chemopreventive Effect of Que
"highlight2" >GSR↑,
"highlight2" >IGF-1R↓, IGFIR, AKT, AR, cell proliferative and anti-apoptotic proteins were increased in cancer-induced group whereas supplement of quercetin decreased its expression.
"highlight2" >Akt↓,
"highlight2" >AR↓, Protein expressions of AR were increased in both VP and DLP of cancer-induced rats and decreasedin quercetin supplemented rats.Fig. 2. Effect of quercetin on mRNA expressions of IGFIR, Bax, Bcl2, Caspase-3 and -8 in VP of cancer-induced male rats.G.
"highlight2" >TumCP↓,
"highlight2" >lipid-P↓,
"highlight2" >H2O2↓,
"highlight2" >Raf↓, Raf-1 and pMEK pro-tein expressions were increased significantly in cancer-induced rats compared to control whereas simultaneous quercetin treatment decreased the expressions
"highlight2" >p‑MEK↓,
"highlight2" >Bcl-2↑, Bcl2, Bcl-xl were significantly increased and apoptotic protein caspase-3,-8,-9 expressions were significantly decreased in cancer-induced rats compared to control in both ventral and dorsolateral prostate. But,this was the other way around when s
"highlight2" >Bcl-xL↑,
"highlight2" >Casp3↑,
"highlight2" >Casp8↑,
"highlight2" >Casp9↑,

80- QC,    Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway
- in-vitro, Pca, PC3
"highlight2" >Vim↓, Quercetin prevented EGF-induced expression of N-cadherin and vimentin and increased the expression of E-cadherin in PC-3 cells
"highlight2" >ERK↓,
"highlight2" >Snail↓,
"highlight2" >Slug↓,
"highlight2" >Twist↓,
"highlight2" >EGFR↓, quercetin prevents EGF-induced EMT via EGFR/PI3k/Akt/ERK1/2 pathway and by suppressing transcriptional repressors Snail, Slug and Twist in PC-3 cells.
"highlight2" >p‑Akt↓,
"highlight2" >EGFR↓,
"highlight2" >N-cadherin↓,
"highlight2" >TumMeta↓, concluded from the present study that quercetin may prevent cancer metastasis by targeting EMT.
"highlight2" >EMT↓,

81- QC,  EGCG,    Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
- in-vivo, Pca, NA
"highlight2" >COMT↓,
"highlight2" >MRP1↓,
"highlight2" >Ki-67↓,
"highlight2" >Bax:Bcl2↑,
"highlight2" >AR↓, significant increase in the inhibition of proliferation, androgen receptor (AR) and phosphatidylinositol 3-kinases (PI3K)/Akt signaling, and stimulation of apoptosis.
"highlight2" >Akt↓,
"highlight2" >p‑ERK↓, ERK1/2
"highlight2" >COMT↓, Increased inhibition of COMT protein and mRNA expression and MRP1 protein expression
"highlight2" >eff↑, Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
"highlight2" >chemoPv↑, novel regimen by combining GT and Q to improve chemoprevention in a non-toxic manner and warrant future studies in humans.
"highlight2" >BioAv↑, Increased bioavailability and decreased methylation of GTPs

82- QC,  ATG,    Arctigenin in combination with quercetin synergistically enhances the anti-proliferative effect in prostate cancer cells
- in-vitro, Pca, LNCaP
"highlight2" >AR↓,
"highlight2" >PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
"highlight2" >miR-21↓,
"highlight2" >STAT3↓,
"highlight2" >BAD↓,
"highlight2" >PRAS40↓,
"highlight2" >GSK‐3β↓,
"highlight2" >PSA↓,
"highlight2" >NKX3.1↑,
"highlight2" >Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
"highlight2" >miR-19b↓,
"highlight2" >miR-148a↓,
"highlight2" >AMPKα↓,
"highlight2" >TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
"highlight2" >chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
"highlight2" >TumCMig↓, Enhanced inhibition of cell migration

83- QC,    Quercetin induces p53-independent apoptosis in human prostate cancer cells by modulating Bcl-2-related proteins: a possible mediation by IGFBP-3
- in-vitro, Pca, PC3
"highlight2" >Bcl-2↓,
"highlight2" >Bcl-xL↓,
"highlight2" >BAX↑, In quercetin-treated PC-3 cells, an increase in Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein were observed.
"highlight2" >IGFBP3↑, There was a twofold increase in IGFBP-3 level in conditioned media of 100 microM quercetin-treated cells.

3602- QC,    The flavonoid quercetin ameliorates Alzheimer's disease pathology and protects cognitive and emotional function in aged triple transgenic Alzheimer's disease model mice
- in-vivo, AD, NA
"highlight2" >*BACE↓, significant reduction in the paired helical filament (PHF), β-amyloid (βA) 1–40 and βA 1–42 levels and a decrease in BACE1-mediated cleavage of APP (into CTFβ).
"highlight2" >*cognitive↑, protects cognitive and emotional function in aged 3xTg-AD mice.
"highlight2" >*ROS↓, These potential uses may be due to its high oxygen radical scavenging activity or its ability to inhibit xanthine oxidase and lipid peroxidation in vitro
"highlight2" >*lipid-P↓,
"highlight2" >*iNOS↓, inhibiting iNOS (Martinez-Florez et al., 2005) and regulating the expression of COX-2
"highlight2" >*COX2↓,
"highlight2" >*BBB↑, ability to penetrate the blood brain barrier
"highlight2" >*neuroP↑, n addition to neuroprotection, quercetin has been suggested to exert other beneficial effects on the central nervous system (CNS), such as anti-anxiety and cognitive enhancement, by stimulating or inhibiting enzyme activities/signal transduction path
"highlight2" >*other↓, remarkable reduction in the βA 1–40 and βA 1–42 levels in the hippocampus of the quercetin-treated 3xTg-AD mice compared to the vehicle-treated 3xTg-AD mice
"highlight2" >*memory↑, Quercetin improves the spatial learning and memory task performance of 3xTg-AD mice

3609- QC,    Factors modulating bioavailability of quercetin-related flavonoids and the consequences of their vascular function
- Review, Var, NA
"highlight2" >*BioAv↑, Onion may be superior to quercetin supplement from the viewpoint of quercetin bioavailability, probably because the food matrix enhances the intestinal absorption of quercetin.

3608- QC,    Chronic diseases, inflammation, and spices: how are they linked?
- Review, Var, NA
"highlight2" >AntiCan↑, anti-cancer, anti-inflammatory, and anti-oxidant properties of this phytochemical are demonstrated by numerous studies
"highlight2" >*Inflam↓,
"highlight2" >*antiOx↑,
"highlight2" >*NF-kB↓, ability to downregulate NF-κB and MAPK pathways and enhance PI3K/Akt and Nrf2 pathways
"highlight2" >*MAPK↓,
"highlight2" >*PI3K↑,
"highlight2" >*Akt↑,
"highlight2" >*NRF2↑,

3607- QC,    Mechanisms of Neuroprotection by Quercetin: Counteracting Oxidative Stress and More
- Review, AD, NA - Review, Park, NA
"highlight2" >*neuroP↑, supportive evidence for neuroprotective effects of quercetin
"highlight2" >*NRF2↑, nduction of Nrf2-ARE and induction of the antioxidant/anti-inflammatory enzyme paraoxonase 2 (PON2).
"highlight2" >*PONs↑,
"highlight2" >*antiOx↑,
"highlight2" >*Inflam↓,
"highlight2" >*SIRT1↑, quercetin has been shown to activate sirtuins (SIRT1), to induce autophagy, and to act as a phytoestrogen, all mechanisms by which quercetin may provide its neuroprotection.
"highlight2" >*eff↑, Additionally, coadministration of quercetin and alpha-tocopherol has been shown to increase the transport of quercetin across the blood-brain barrier
"highlight2" >*ROS↓, was shown to protect rodents from oxidative stress
"highlight2" >*cognitive↑, quercetin ameliorates Alzheimer's disease pathology and related cognitive deficits in an aged triple transgenic Alzheimer's disease mouse model
"highlight2" >*eff↑, combined oral supplementation of quercetin and fish oil enhanced neuroprotection in rats exposed to 3-nitropropionic acid
"highlight2" >*lipid-P↓, Decreased lipid perox. in hippocampus;
"highlight2" >*GSH↑, Decreased reduction of GSH, GPx (5, 50 mg/kg)
"highlight2" >*GPx↑,
"highlight2" >*SOD↑, Diminished reduction of DA levels, SOD, and GPx
"highlight2" >*NRF2↑, Quercetin has been shown to counteract oxidative stress-induced cellular damage by activating the Nrf2-ARE pathway

3606- QC,    The Effect of Quercetin on Inflammatory Factors and Clinical Symptoms in Women with Rheumatoid Arthritis: A Double-Blind, Randomized Controlled Trial
- Trial, Arthritis, NA
"highlight2" >*motorD↑, Quercetin supplementation for 8 weeks significantly reduced EMS, morning pain, and after-activity pain
"highlight2" >*Pain↓,
"highlight2" >*TNF-α↓, Plasma hs-TNFα level was significantly reduced in the quercetin group compared to placebo
"highlight2" >*IL8↓, Other studies showed that 30 mM quercetin decreased gene expression and production of IL-8, 1L-6, IL-1b, and TNFa, which are the major inflammatory cytokines i
"highlight2" >*IL6↓,
"highlight2" >*IL1β↓,
"highlight2" >*NF-kB↓, also inhibited the activity of NF-kB and P38-kinase protein
"highlight2" >*p38↓,

3605- QC,    Protective effect of quercetin in primary neurons against Aβ(1–42): relevance to Alzheimer's disease
- Review, AD, NA
"highlight2" >*Aβ↓, Pretreatment of primary hippocampal cultures with quercetin significantly attenuated Aβ(1–42)-induced cytotoxicity, protein oxidation, lipid peroxidation and apoptosis
"highlight2" >*ROS↓,
"highlight2" >*lipid-P↓,
"highlight2" >*Apoptosis↓,

3604- QC,    Quercetin enrich diet during the early-middle not middle-late stage of alzheimer’s disease ameliorates cognitive dysfunction
- in-vivo, AD, NA
"highlight2" >*cognitive↑, early-middle stage of AD pathological development period ameliorates cognitive dysfunction and the protection effect was mainly related to increased Aβ clearance and reduced astrogliosis.
"highlight2" >*Aβ↓, Quercetin enrich diet prevented cognitive dysfunction through increasing Aβ clearance and astrocyte function. has been demonstrated that it could inhibit the aggregation of Aβ
"highlight2" >*neuroP↑, quercetin may have neuro-protective effects and slow down the progression of degenerative diseases
"highlight2" >*BACE↓, The results showed that the protein level of CTFβ and BACE1 was decreased
"highlight2" >*p‑SMAD2↓, protein level of p-Smad2 and p-STAT3 were decreased in quercetin enrich diet
"highlight2" >*p‑STAT3↓,
"highlight2" >*SPARC↓, quercetin enrich diet (1 month-9 months) significantly reduced the mRNA and protein level of Hevin and SPARC compared with normal diet.

3603- QC,    Mechanism of quercetin therapeutic targets for Alzheimer disease and type 2 diabetes mellitus
- Review, AD, NA - Review, Diabetic, NA
"highlight2" >*MAPK↓, We speculate that quercetin may have therapeutic applications in T2DM and AD by targeting MAPK signaling,
"highlight2" >*neuroP↑, Quercetin has also shown anti-dementia and neuroprotective efficacies in models of dementia/AD and ischemia–reperfusion injury
"highlight2" >*ROS↓, mitigating neuronal oxidative stress and neuroinflammation
"highlight2" >*Akt↓, MAPK1 (degree = 18), AKT1 (degree = 15), PIK3R1 (degree = 14), IL6 (degree = 13), PRKCB (degree = 12), TNF, VEGFA, EGFR, CASP3, BCL2, and IL1B
"highlight2" >*PI3K↓,
"highlight2" >*IL6↓,
"highlight2" >*TNF-α↓,
"highlight2" >*VEGF↓,
"highlight2" >*EGFR↓,
"highlight2" >*Casp3↓,
"highlight2" >*Bcl-2↓,
"highlight2" >*IL1β↓,

3611- QC,    Quercetin and vitamin C supplementation: effects on lipid profile and muscle damage in male athletes
- Trial, Nor, NA
"highlight2" >*eff↝, Quercetin and vitamin C supplementation may not be beneficial in lipid profile improvement, although it may reduce induce muscle damage and body fat percent.
"highlight2" >*LDH↓, LDH values decreased significantly (P = 0.048) in “Quercetin + Vit C” group

3601- QC,    Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid
- Review, Var, NA - Review, AD, NA
"highlight2" >*Inflam↓, known for its anti-inflammatory, antihypertensive, vasodilator effects, antiobesity, antihypercholesterolemic and antiatherosclerotic activities
"highlight2" >*cardioP↑, beneficial effects include cardiovascular protection, anticancer, antitumor, anti-ulcer, anti-allergy, anti-viral, anti-inflammatory activity, anti-diabetic, gastroprotective effects, antihypertensive, immunomodulatory, and anti-infective.
"highlight2" >AntiCan↑,
"highlight2" >AntiTum↑,
"highlight2" >*neuroP↑, The consumption of flavonoids rich food limits neurodegeneration and to reverse age-dependent loss in cognitive performance.
"highlight2" >*cognitive↑,
"highlight2" >*ROS↓, It is known to protect brain cells against the oxidative stress, which damages tissue leading to Alzheimer and other neurological conditions
"highlight2" >*BP↓, Quercetin supplementation (150 mg/day) reduced systolic blood pressure and plasma oxidized LDL concentrations in overweight subjects
"highlight2" >*LDL↓,

3534- QC,  Lyco,    Synergistic protection of quercetin and lycopene against oxidative stress via SIRT1-Nox4-ROS axis in HUVEC cells
- in-vitro, Nor, HUVECs
"highlight2" >*ROS↓, especially quercetin-lycopene combination (molar ratio 5:1), prevented the oxidative stress in HUVEC cells by reducing the reactive oxygen species (ROS) and suppressing the expression of NADPH oxidase 4 (Nox4), a major source of ROS production.
"highlight2" >*NOX4↓, Quercetin-lycopene combination could interact with SIRT1 to inhibit Nox4 and prevent endothelial oxidative stress
"highlight2" >*Inflam↓, quercetin-lycopene combination downregulated inflammatory genes induced by H2O2, such as IL-17 and NF-κB.
"highlight2" >*NF-kB↓, NF-κB p65 was activated by H2O2 but inhibited by the quercetin-lycopene combination.
"highlight2" >*p65↓,
"highlight2" >*SIRT1↑, quercetin and lycopene combination promoted the thermostability of Sirtuin 1 (SIRT1) and activated SIRT1 deacetyl activity
"highlight2" >*cardioP↑, The cardioprotective role of SIRT1
"highlight2" >*IL6↓, LYP: Q = 1:5), interacted with deacetylase SIRT1 to inhibit NF-κB p65 and Nox4 enzyme, downregulated inflammatory cytokines such as IL-6 and pro-inflammatory enzymes such as COX-2, and suppressed ROS elevation activated by H2O2.
"highlight2" >*COX2↓,

3381- QC,    Quercetin induces cell death in cervical cancer by reducing O-GlcNAcylation of adenosine monophosphate-activated protein kinase
- in-vitro, Cerv, HeLa
"highlight2" >SREBP1↓, quercetin treatment decreased the immunoreactivities of OGT and SREBP-1 in HeLa cells. Our
"highlight2" >TumCP↓, Quercetin decreased cell proliferation and induced cell death, but its effect on HaCaT cells was lower than that on HeLa cells.
"highlight2" >TumCD↑,
"highlight2" >AMPK↑, Quercetin decreased the expression of global O-GlcNAcylation and increased AMPK activation by reducing the O-GlcNAcylation of AMPK
"highlight2" >SREBP1↓, Once activated, AMPK regulates various proteins involved in metabolism, which suppress energy consumption and cellular growth, such as sterol regulatory element binding protein 1 (SREBP-1
"highlight2" >FASN↓, FAS and ACC were significantly decreased in cells treated with quercetin
"highlight2" >ACC↓,

3380- QC,    Quercetin as a JAK–STAT inhibitor: a potential role in solid tumors and neurodegenerative diseases
- Review, Var, NA - Review, Park, NA - Review, AD, NA
"highlight2" >JAK↓, plant polyphenols, especially quercetin, exert their inhibitory effects on the JAK–STAT pathway through known and unknown mechanisms.
"highlight2" >STAT↓,
"highlight2" >Inflam↓, quercetin significantly reduced levels of inflammation moderators, including NO synthase, COX-2, and CRP, in a human hepatocyte-derived cell line
"highlight2" >NO↓,
"highlight2" >COX2↓,
"highlight2" >CRP↓,
"highlight2" >selectivity↑, , quercetin is not harmful to healthy cells, while it can impose cytotoxic effects on cancer cells through a variety of mechanisms,
"highlight2" >*neuroP↑, Alzheimer’s disease because of its antioxidant and anti-inflammatory activity.
"highlight2" >STAT3↓, demonstrated as a suppressor of the STAT3 activation signaling pathway
"highlight2" >cycD1/CCND1↓, Rb phosphorylation, cyclin D1 expression, and MMP-2 secretion are inhibited by 48 h treatment with 25 µM quercetin in T98G and U87 GBM cell lines
"highlight2" >MMP2↓,
"highlight2" >STAT4↓, by inhibiting IL-12-induced tyrosine phosphorylation of STAT3, STAT4, JAK2, and TYK2, quercetin inhibits the proliferation of T cells and differentiation of Th1
"highlight2" >JAK2↓,
"highlight2" >TumCP↓,
"highlight2" >Diff↓,
"highlight2" >*eff↑, administration of quercetin with piperine alone and in combination significantly prevented neuroinflammation via reducing the levels of IL-6, TNF-α (two potent activators of the JAK–STAT pathway), and IL-1β in PD in experimental rats
"highlight2" >*IL6↓,
"highlight2" >*TNF-α↓,
"highlight2" >*IL1β↓,
"highlight2" >*Aβ↓, quercetin suppressing β-secretase (an enzyme engaged in Aβ formation) and aggregation of Aβ

3379- QC,    The Effect of Quercetin Nanosuspension on Prostate Cancer Cell Line LNCaP via Hedgehog Signaling Pathway
- in-vitro, Pca, LNCaP
"highlight2" >tumCV↓, The cell viability gradually decreased with increased concentration of quercetin nanoparticles.
"highlight2" >HH↓, To sum up, nanoparticles of quercetin improved the inhibitory role in progression of PCa on cell line LNCaP via Hh signaling pathway. targeted inhibition of the Hh pathway could also be an efficient way to stop PCa progression.

3378- QC,    CK2 and PI3K are direct molecular targets of quercetin in chronic lymphocytic leukaemia
- in-vitro, AML, NA
"highlight2" >CK2↓, We demonstrated that the activity of protein kinase CK2, which positively triggers PI3K/Akt pathway by inactivating PTEN phosphatase, is inhibited by quercetin
"highlight2" >PI3K↓, The combined inhibition of CK2 and PI3K kinase activities by quercetin restored ABT-737 sensitivity and increased lethality in human leukemia cells.
"highlight2" >TumCD↑,
"highlight2" >Akt↓, Quercetin inhibits the PI3K-Akt-Mcl-1 pathway
"highlight2" >Mcl-1↓,
"highlight2" >PTEN↑, Inhibition of CK2 can rescue PTEN activity increasing apoptosis in CLL

3377- QC,    Quercetin inhibits a large panel of kinases implicated in cancer cell biology
"highlight2" >PDGF↓, decreased the activity of 16 kinases by more than 80%, including ABL1, Aurora-A, -B, -C, CLK1, FLT3, JAK3, MET, NEK4, NEK9, PAK3, PIM1, RET, FGF-R2, PDGF-Rα and -Rß.
"highlight2" >FLT3↓,
"highlight2" >JAK3↓,
"highlight2" >MET↓,
"highlight2" >RET↓,
"highlight2" >FGFR2↓,
"highlight2" >other↓, Quercetin markedly inhibited the activity of both the CLK1 and CLK4 kinases at 2 uM but inhibited to a much lower extent the activities of the CLK2 and CLK3 kinases

3339- QC,    Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas
- in-vitro, GBM, C6 - in-vitro, GBM, IMR32
"highlight2" >BBB↑, capacity to cross the blood–brain barrier
"highlight2" >tumCV↓, Quercetin significantly reduced the viability and migration of cells in an ROS-dependent manner with the concomitant inhibition of Rac1/p66Shc expression and ROS production in naïve and Rac1/p66Shc-transfected cell lines, suggestive of preventing Rac
"highlight2" >TumCMig↓,
"highlight2" >Rac1↓,
"highlight2" >p66Shc↓,
"highlight2" >ROS↓, treatment of cells with quercetin not only reduced the levels of ROS (Figure 4) but also showed a significant inhibition of p66Shc/Rac1

4787- QC,    Quercetin: A Phytochemical with Pro-Apoptotic Effects in Colon Cancer Cells
- Review, CRC, NA
"highlight2" >Inflam↓, quercetin, has been shown to have anti-inflammatory and anti-carcinogenic effects
"highlight2" >AntiCan↑,
"highlight2" >Apoptosis↑, nduce apoptosis via the mitochondrial apoptotic pathway by causing changes in the mitochondrial membrane potential.
"highlight2" >MMP↓,
"highlight2" >P53↑, quercetin also induces apoptosis through the activation of p53, increasing the expression of pro-apoptotic molecules such as Bax, caspase-3, caspase-9, and inhibition of anti-apoptotic proteins such as Bcl-2
"highlight2" >BAX↑,
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >Bcl-2↓,
"highlight2" >NF-kB↓, Quercetin might exert anti-inflammatory properties by suppressing NF-kB translocation and the expression of pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), IL-1b
"highlight2" >IL6↓,
"highlight2" >IL1β↓,
"highlight2" >*antiOx↑, Quercetin is a powerful antioxidant and lipid peroxidation inhibitor, thanks to its catechol and hydroxyl group configuration, its capacity to scavenge free radicals and to bind metal ions.
"highlight2" >*lipid-P↓,
"highlight2" >*ROS↓,
"highlight2" >MAPK↓, Quercetin has the potential to exert an anti-cancer effect by inhibiting important signaling pathways in carcinogenesis such as MAPK, JAK-STAT, and PI3K-Akt.
"highlight2" >JAK↓,
"highlight2" >STAT↓,
"highlight2" >PI3K↓,
"highlight2" >Akt↓,
"highlight2" >chemoP↑, Quercetin is a lipophilic compound which can cross the cell membrane and activate multiple intracellular signaling pathways in chemoprevention
"highlight2" >ROS⇅, dual function as a pro-oxidant or anti-oxidant. Oxidative stress caused by ROS species causes DNA damage and mutation development.
"highlight2" >DNAdam↑,
"highlight2" >ChemoSen↝, Therefore, it is thought that quercetin can be applied as a supplement in cancer treatment in combination with existing chemotherapies.

5031- QC,    Different roles of Nrf2 and NFKB in the antioxidant imbalance produced by esculetin or quercetin on NB4 leukemia cells
- in-vitro, AML, APL NB4
"highlight2" >NRF2↓, Quercetin increased the levels of Nrf2 in the cytosol reducing them in the nucleus
"highlight2" >ROS↑, AI summary: Suppresses NRF2 activity, Leads to: ↓ antioxidant gene expression, ↑ ROS accumulation, Oxidative stress–driven apoptosis
"highlight2" >Apoptosis↑,

5030- QC,    Quercetin-derived microbial metabolite DOPAC potentiates CD8+ T cell anti-tumor immunity via NRF2-mediated mitophagy
- in-vivo, Nor, NA
"highlight2" >*MitoP↑, DOPAC promotes mitophagy by preventing KEAP1-mediated degradation of NRF2
"highlight2" >*NRF2↑, Mechanistically, DOPAC directly binds to Kelch-like epichlorohydrin-associated protein 1 (KEAP1), disrupting its interaction with nuclear factor erythroid 2-related factor 2 (NRF2) and preventing KEAP1-mediated degradation of NRF2 in CD8+ T cells.
"highlight2" >eff↑, DOPAC synergizes with immune checkpoint blockade to suppress tumor growth.
"highlight2" >*eff↓, In this study, we found that eliminating gut microbiota with antibiotics disrupted the anti-tumor effect of dietary quercetin.
"highlight2" >*GutMicro↑, these findings highlight the role of gut microbiota in utilizing dietary quercetin to counteract tumors, suggesting gut microbe-derived DOPAC as a promising candidate for cancer therapy and a potential amplifier of ICB therapy.

5029- QC,    Molecular mechanisms of action of quercetin in cancer: recent advances
- in-vitro, Liver, HepG2
"highlight2" >NRF2↑, Quercetin modulates OTA-induced oxidative stress and redox signaling in HepG2 cells—up regulation of Nrf2 expression and down regulation of NF-kβ and COX-2
"highlight2" >NF-kB↓,
"highlight2" >COX2↓,

5028- QC,    Quercetin inhibited LPS-induced cytokine storm by interacting with the AKT1-FoxO1 and Keap1-Nrf2 signaling pathway in macrophages
- vitro+vivo, Nor, RAW264.7
"highlight2" >*ROS↓, quercetin can reduce ROS through the Keap1-Nrf2 signaling pathway
"highlight2" >*Keap1↓,
"highlight2" >*NRF2↑,

5027- QC,    NRF2 Is Targeted By the Polyphenol Quercetin and Induces Apoptosis, in Part, through up Regulation of Pro Apoptotic Mirs
- in-vivo, AML, NA
"highlight2" >HDAC4↓, Qu treatment (50 µM Qu) for 48h downregulated HDAC4, NRF2 and p-NRF2 at protein levels (p<0.05; p<0.005; p<0.005 respectively).
"highlight2" >NRF2↓,
"highlight2" >p‑NRF2↓,
"highlight2" >miR-133a-3p↑, miR-1, miR-133a/b, which target anti-apoptotic genes and miR-206, a pro apoptotic miR, were validated in xenograft model samples, resulting in a significant up-regulation of the expression levels in treated animals
"highlight2" >miR-206↑,

5026- QC,    Quercetin induces ferroptosis in gastric cancer cells by targeting SLC1A5 and regulating the p-Camk2/p-DRP1 and NRF2/GPX4 Axes
- in-vitro, GC, NA
"highlight2" >SLC1A5↓, We demonstrated that Quer inhibits SLC1A5 expression
"highlight2" >ROS↑, we found that Quer altered the intracellular ROS levels, antioxidant system protein expression levels, and iron content.
"highlight2" >Iron↓, Quer increased the intracellular iron content by inhibiting SLC1A5
"highlight2" >NRF2↓, Mechanistically, Quer binds to SLC1A5, inhibiting the nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), resulting in decreased xCT/GPX4 expression.
"highlight2" >GPx4↓,
"highlight2" >Ferroptosis↑, These three changes collectively led to ferroptosis in GC cells

5025- QC,    New perspectives on the therapeutic potential of quercetin in non-communicable diseases: Targeting Nrf2 to counteract oxidative stress and inflammation
- Review, Nor, NA
"highlight2" >*antiOx↑, Quercetin (Que) is a widely available flavonoid that has significant antioxidant and anti-inflammatory properties. It modulates the Nrf2 signaling pathway to ameliorate oxidative stress and inflammation.
"highlight2" >*Inflam↓,
"highlight2" >*NRF2↓,
"highlight2" >*ROS↓, Que modulates mitochondrial function, apoptosis, autophagy, and cell damage biomarkers to regulate oxidative stress and inflammation, highlighting its efficacy as a therapeutic agent against NCDs.
"highlight2" >*cardioP↑, Nrf2 promotes the proliferation and repair of vascular smooth muscle cells, effectively restoring the optimal structure and function of blood vessels to improve cardiovascular health.
"highlight2" >*HO-1↑, Que interacts with antioxidant enzymes such as HO-1, CAT, and glutathione peroxidase (GSH-PX), and enhances their free radical scavenging activity
"highlight2" >*Catalase↑,
"highlight2" >*GPx↑,
"highlight2" >*NQO1↑, This process upregulates the expressions of key antioxidant and detoxification genes, such as HO-1 and NQO1, thereby inhibiting excessive intracellular ROS production.
"highlight2" >*SIRT1↑, Que mediated by the activation of the Sirt1/Nrf2/HO-1 pathway,

4827- QC,  CUR,    Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin
- Review, Var, NA
"highlight2" >*AntiCan↑, their anti-cancer effects, but also with regard to their anti-diabetic, anti-obesity, anti-inflammatory, and anti-bacterial actions.
"highlight2" >*Inflam↓,
"highlight2" >*Bacteria↓,
"highlight2" >*AntiDiabetic↑,
"highlight2" >*ROS↓, suppression of ROS formation via the inhibition of the enzyme activities involved in their production, or via scavenging ROS directly by acting as hydrogen donors; the chelation of the metal ions that induce ROS production;
"highlight2" >*SOD↑, quercetin can eliminate free radicals and help maintain a stable redox state in cells by increasing anti-oxidant enzymes, such as superoxide dismutase (SOD), and catalase expressions, as well as the level of reduced glutathione (GSH)
"highlight2" >*Catalase↑,
"highlight2" >*GSH↑,
"highlight2" >*NRF2↑, Quercetin can protect human granulosa cells from oxidative stress by inducing Nrf2 expression at both the gene and protein levels, which in turn induces the anti-oxidant thioredoxin (Trx) system.
"highlight2" >*Trx↑,
"highlight2" >*IronCh↑, pure curcumin, a metal chelator, directly removes ROS and regulates numerous enzymes.
"highlight2" >*MDA↑, It has the potential to reduce the concentration of malondialdehyde (MDA) in serum and increase the total anti-oxidant potential
"highlight2" >cycD1/CCND1↓, Cyclin D1 expression was significantly decreased in quercetin-treated ovarian SKOV-3 cells, but not in cisplatin (CDDP)-resistant SKOV3/CDDP cells.
"highlight2" >PI3K↓, The levels of PI3K and phospho-Akt were decreased in curcumin-treated SKOV3 cells, which in turn increased caspase-3 and Bax levels.
"highlight2" >Casp3↑,
"highlight2" >BAX↑,
"highlight2" >ChemoSen↑, Curcumin enhanced the efficacy of chemotherapy in colorectal cancer cells.
"highlight2" >ROS↑, suggesting that quercetin-induced cytotoxicity and autophagy were initiated by the generation of ROS
"highlight2" >eff↑, quercetin or curcumin with chemotherapeutic agents, as shown below, considerably enhances the antitumor potencies of doxorubicin (DOX) and cisplatin.
"highlight2" >MMP↓, The synergistic treatment with curcumin and quercetin inhibited the cell proliferation associated with the loss of mitochondrial membrane potential (ΔΨm), the release of cytochrome c, a decrease in AKT and ERK phosphorylation in MGC803 human gastric
"highlight2" >Cyt‑c↑,
"highlight2" >Akt↓,
"highlight2" >ERK↓,

3610- QC,    Bioavailability of quercetin: problems and promises
"highlight2" >*BioAv↓, application of QC in pharmaceutical field is limited due to its poor solubility, low bioavailability, poor permeability and instability.
"highlight2" >*BioAv↑, Various types of lipid formulations, such as liposome, lipid nanoparticle, phospholipid complex etc., are suitable for the delivery of an active form of QC
"highlight2" >*BioAv↑, QC-Encapsulated Polymer Nanoparticles

4686- QC,    Quercetin suppresses endometrial cancer stem cells via ERα-mediated inhibition of STAT3 signaling
- in-vitro, EC, EMN8 - in-vitro, EC, EMN21
"highlight2" >CSCs↓, downregulated the expression of stemness markers, including ALDH1A1, c-Myc, Nanog, and Oct4
"highlight2" >ALDH1A1↓, the expression of stemness markers—ALDH1A1, c-Myc, Nanog and Oct4 was examined, and as expected, all were downregulated following Quercetin treatment
"highlight2" >cMyc↓,
"highlight2" >Nanog↓,
"highlight2" >OCT4↓,
"highlight2" >STAT3↓, Quercetin suppressed STAT3/JAK2 phosphorylation and subsequently inhibited the transcriptional activity of STAT3’s downstream target gene, Oct4
"highlight2" >JAK2↓,
"highlight2" >STAT3↓,
"highlight2" >eff↑, Quercetin exerts inhibitory roles via the presence of estrogen receptor (ER) in CSCs derived from endometrial cancer cells

4665- QC,  Ash,  Api,    Targeting cancer stem cells by nutraceuticals for cancer therapy
- Review, Var, NA
"highlight2" >CSCs↓, we will describe the some natural chemopreventive agents that target CSCs in a variety of human malignancies, including soy isoflavone, curcumin, resveratrol, tea polyphenols, sulforaphane, quercetin, indole-3-carbinol, 3,3′-diindolylmethane, withafe

4297- QC,    Quercetin attenuates tau hyperphosphorylation and improves cognitive disorder via suppression of ER stress in a manner dependent on AMPK pathway
- in-vitro, AD, SH-SY5Y
"highlight2" >*AMPK↑, administration of quercetin enhanced AMPK activity, inhibited IRE1α and PERK phosphorylation, NLRP3 expression and tau phosphorylation
"highlight2" >*IRE1↓,
"highlight2" >*p‑PERK↓,
"highlight2" >*p‑tau↓,
"highlight2" >*cognitive↑, and improved cognitive disorder in mice exposed to high fat diets
"highlight2" >*antiOx↑, exert anti-oxidative, anti-ER stress, anti-inflammatory activities and regulating glucose homeostasis, which can prevent neurodegenerative disorders, diabetes, and obesity
"highlight2" >*ER Stress↓,
"highlight2" >*Inflam↓,
"highlight2" >*neuroP↑,
"highlight2" >*TXNIP↓, Quercetin and quercetin-3-O-glucuronide suppressed ER stress with decreased phosphorylation of IRE1α and PERK, thereby inhibited TXNIP and NLRP3 inflammasome activation,
"highlight2" >*NLRP3↓, effectively protected neuronal cells from inflammatory insult by blocking ER stress/NLRP3 inflammasome activation.

4296- QC,    A Flavonoid on the Brain: Quercetin as a Potential Therapeutic Agent in Central Nervous System Disorders
- Review, AD, NA
"highlight2" >*Inflam↓, Commonly recognized as an anti-inflammatory agent, quercetin not only limits capillary vessel permeability by inhibiting hyaluronidase but also blocks cyclooxygenases and lipoxygenases.
"highlight2" >*COX2↓,
"highlight2" >*5LO↓,
"highlight2" >*antiOx↑, well-known antioxidant (recognized as one of the most potent antioxidant flavonoids, considered to be stronger than vitamin C or tocopherols
"highlight2" >*BioAv↝, Quercetin-Loaded Nanocarriers—New Delivery to Better Availability
"highlight2" >*GPx↑, Que at two higher doses improved the antioxidant enzymes (glutathione peroxidase, superoxide dismutase (SOD), Na+/K+-ATPase) supplies and elevated the levels of ACh
"highlight2" >*SOD↑,
"highlight2" >*Ach↑,
"highlight2" >*4-HNE↓, whereas the levels of peroxidation product, 4-HNE, were reduced in the striatum
"highlight2" >*CREB↑, A recent study showed a positive influence on the expression of the hippocampal FoxG1/CREB/BDNF signaling pathway [93]
"highlight2" >*BDNF↑,
"highlight2" >*ROS↓, quercetin exerted antioxidant (reducing ROS, increasing SOD, GST, GSH activity) as well as anti-inflammatory activity (suppressing IL-1β, IL-6, TNF-α, COX-2, microglial activation) [
"highlight2" >*GSH↑,
"highlight2" >*IL1β↓,
"highlight2" >*IL6↓,
"highlight2" >*TNF-α↓,

4162- QC,    Quercetin attenuates cell apoptosis in focal cerebral ischemia rat brain via activation of BDNF-TrkB-PI3K/Akt signaling pathway
- in-vivo, Stroke, NA
"highlight2" >*neuroP↑, Quercetin significantly improved neurological function, while it decreased the infarct volume and the number of TdT mediated dUTP nick end labeling positive cells in MCAO rats.
"highlight2" >*BDNF↑, The protein expression of BDNF, TrkB and p-Akt also increased in the quercetin treated rats.
"highlight2" >*TrkB↑,
"highlight2" >*p‑Akt↑,

3796- QC,  BBR,    Biomarker discovery and phytochemical interventions in Alzheimer's disease: A path to therapeutic advances
- Review, AD, NA
"highlight2" >*CDK5↓, BAD, CDK5, FN1, ITGA4, and MAPK9 were identified. Quercetin and Berberine have shown significant binding affinities to these biomarkers

3376- QC,    Inhibiting CDK6 Activity by Quercetin Is an Attractive Strategy for Cancer Therapy
- in-vitro, BC, MCF-7 - in-vitro, Lung, A549
"highlight2" >CDK6↓, The cell-based protein expression studies in the breast (MCF-7) and lung (A549) cancer cells revealed that the treatment of quercetin decreases the expression of CDK6.
"highlight2" >tumCV↓, Quercetin also decreases the viability and colony formation potential of selected cancer cells.
"highlight2" >Apoptosis↑, Moreover, quercetin induces apoptosis, by decreasing the production of reactive oxygen species and CDK6 expression
"highlight2" >ROS↓,
"highlight2" >eff↑, Interestingly, when used in combination, quercetin increases the efficiencies of other anticancer molecules like losartan, paclitaxel, and resveratrol in different cancers

3349- QC,    Quercetin Exerted Protective Effects in a Rat Model of Sepsis via Inhibition of Reactive Oxygen Species (ROS) and Downregulation of High Mobility Group Box 1 (HMGB1) Protein Expression
- in-vivo, Sepsis, NA
"highlight2" >*Sepsis↓, results showed that quercetin reduced the tissue edema, congestion, and hemorrhage, increased the alveolar volume, and helped to maintain the lung anatomy of septic rats.
"highlight2" >*ROS↓, Admistration of quercetin at the dosage of 15 and 20 mg/kg to septic rats caused significant reduction in the ROS levels.
"highlight2" >*SOD↑, The results showed that administration of quercetin at the dosage of 15 and 5 mg/kg to septic rats caused a significant increase in SOD, CAT, and APX expression levels
"highlight2" >*Catalase↑,
"highlight2" >*HMGB1↓, quercetin caused a significant decrease in HMGB1 protein levels
"highlight2" >*Inflam↓, quercetin was found to reduce the inflammation associated with sepsis
"highlight2" >*TAC↑, significant increase in the expression of antioxidant enzymes.

3357- QC,    The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes
- in-vitro, AML, HL-60 - NA, NA, U937
"highlight2" >DNMT1↓, Qu treatment almost eliminates DNMT1 and DNMT3a expression, and this regulation was in part STAT-3 dependent.
"highlight2" >DNMT3A↓,
"highlight2" >HDAC↓, The treatment also downregulated class I HDACs.
"highlight2" >ac‑H3↑, Qu (50 μmol/L) treatment of cell lines for 48 h caused accumulation of acetylated histone 3 and histone 4, resulting in three- to ten fold increases in the promoter region of DAPK1, BCL2L11, BAX, APAF1, BNIP3, and BNIP3L.
"highlight2" >ac‑H4↑,
"highlight2" >BAX↑,
"highlight2" >APAF1↑,
"highlight2" >BNIP3↑,
"highlight2" >STAT3↑, Quercetin downregulates DNMTs and STAT3

3356- QC,    Targeting DNA methyltransferases for cancer therapy
- Review, Var, NA
"highlight2" >DNMTs↓, graphical abstract , Quercetin has been shown to downregulate the expression of DNMTs, such as DNMT1 and DNMT3a (ai)

3355- QC,    Quercetin exhibits cytotoxicity in cancer cells by inducing two-ended DNA double-strand breaks
- in-vitro, Cerv, HeLa
"highlight2" >DNAdam↑, Quercetin induced DNA double-strand break
"highlight2" >ROS↑, Reactive oxygen species accumulated in quercetin-treated HeLa cells.
"highlight2" >*antiOx↑, antioxidant properties
"highlight2" >TOP2↓, Quercetin inhibits Top2 in vitro (Quercetin does not act as a Top2 poison)
"highlight2" >γH2AX↑, quercetin concentrations of 50, 100 or 150 μM, γH2AX fluorescence was noticeably observed

3354- QC,    Quercetin: Its Main Pharmacological Activity and Potential Application in Clinical Medicine
- Review, Var, NA
"highlight2" >*ROS↓, quercetin is the most effective free radical scavenger in the flavonoid family
"highlight2" >*IronCh↓, Chelating metal ions: related studies have confirmed that quercetin can induce Cu2+ and Fe2+ to play an antioxidant role through catechol in its structure.
"highlight2" >*lipid-P↓, quercetin could inhibit Fe2+-induced lipid peroxidation by binding Fe2+ a
"highlight2" >*GSH↑, regulation of glutathione levels to enhance antioxidant capacity.
"highlight2" >*NRF2↑, quercetin upregulates the expression of Nrf2 and nuclear transfer by activating the intracellular p38 MAPK pathway, increasing the level of intracellular GSH
"highlight2" >TumCCA↑, human leukaemia U937 cells, quercetin induces cell cycle arrest at G2 (late DNA synthesis phase)
"highlight2" >ER Stress↑, quercetin can induce ER stress and promote the release of p53, thereby inhibiting the activities of CDK2, cyclin A, and cyclin B, thereby causing MCF-7 breast cancer cells to stagnate in the S phase.
"highlight2" >P53↑,
"highlight2" >CDK2↓,
"highlight2" >cycA1/CCNA1↓,
"highlight2" >CycB/CCNB1↓,
"highlight2" >cycE/CCNE↓, downregulation of cyclins E and D, PNCA, and Cdk-2 protein expression and increased expressions of p21 and p27
"highlight2" >cycD1/CCND1↓,
"highlight2" >PCNA↓,
"highlight2" >P21↑,
"highlight2" >p27↑,
"highlight2" >PI3K↓, quercetin inhibited the PI3K/AKT/mTOR and STAT3 pathways in PEL, which downregulated the expression of survival cell proteins such as c-FLIP, cyclin D1, and cMyc.
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >STAT3↓, in excess of 20 μM by inhibiting STAT3 signalling
"highlight2" >cFLIP↓,
"highlight2" >cMyc↓,
"highlight2" >survivin↓, Lung cancer [27] ↓ Survivin ↑DR5
"highlight2" >DR5↓,
"highlight2" >*Inflam↓, Quercetin has been confirmed to be a long-acting anti-inflammatory substance in flavonoids
"highlight2" >*IL6↓, inhibit IL-8 is stronger and can inhibit IL-6 and increase cytosolic calcium levels
"highlight2" >*IL8↓,
"highlight2" >COX2↓, inhibit the enzymes that produce inflammation (cyclooxygenase (COX) and lipoxygenase (LOX))
"highlight2" >5LO↓,
"highlight2" >*cardioP↑, The protective mechanism of quercetin on the cardiovascular system
"highlight2" >*FASN↓, 25 μM, within 30 minutes could inhibit the synthesis of fatty acids.
"highlight2" >*AntiAg↑, quercetin helps reduce lipid peroxidation, platelet aggregation, and capillary permeability
"highlight2" >*MDA↓, quercetin can decrease the levels of malondialdehyde (MDA)

3353- QC,    Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells
- in-vitro, Oral, KON - in-vitro, Nor, MRC-5
"highlight2" >tumCV↓, reduced the vitality of KON cells and had minimal effect on MRC cells.
"highlight2" >selectivity↑, Owing to the appropriate dosages of quercetin needed to treat these diseases, normal cells do not exhibit any overtly harmful side effects.
"highlight2" >TumCCA↑, quercetin increased the percentage of dead cells and cell cycle arrests in the S and G2/M phases.
"highlight2" >TumCMig↓, quercetin inhibited KON cells’ capacity for migration and invasion in addition to their effects on cell stability and structure
"highlight2" >TumCI↓,
"highlight2" >Apoptosis↑, inducing apoptosis and preventing metastasis, quercetin was found to downregulate the expression of BCL-2/BCL-XL while increasing the expression of BAX.
"highlight2" >TumMeta↓,
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >TIMP1↑, TIMP-1 expression was upregulated while MMP-2 and MMP-9 were downregulated.
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >*Inflam↓, anti-inflammatory, anti-cancer, antibacterial, antifungal, anti-diabetic, antimalarial, neuroprotective, and cardioprotective properties.
"highlight2" >*neuroP↑,
"highlight2" >*cardioP↑,
"highlight2" >p38↓, MCF-7 cells, quercetin successfully decreased the expression of phosphor p38MAPK, Twist, p21, and Cyclin D1
"highlight2" >MAPK↓,
"highlight2" >Twist↓,
"highlight2" >P21↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >Casp3↑, directly aided by the significant increase in caspase-3 and − 9 levels and activities
"highlight2" >Casp9↑,
"highlight2" >p‑Akt↓, High quercetin concentrations also caused an inhibition of Akt and ERK phosphorylation
"highlight2" >p‑ERK↓,
"highlight2" >CD44↓, reduced cell division and triggered apoptosis, albeit to a lesser degree in CD44+/CD24− cells.
"highlight2" >CD24↓,
"highlight2" >ChemoSen↑, combination of quercetin and doxorubicin caused G2/M arrest in T47D cells, and to a lesser amount in cancer stem cells (CSCs) that were isolate
"highlight2" >MMP↓, (lower levels of ΔΨ m), which is followed by the release of Cyto C, AIF, and Endo G from mitochondria, which causes apoptosis and ultimately leads to cell death.
"highlight2" >Cyt‑c↑,
"highlight2" >AIF↑,
"highlight2" >ROS↑, Compared to the control group, quercetin administration significantly raised ROS levels at 25, 50, 100, 200, and 400 µg/mL.
"highlight2" >Ca+2↑, increased production of reactive oxygen species and Ca2+, decreased levels of mitochondrial membrane potential (ΔΨ m),
"highlight2" >Hif1a↓, Quercetin treatment resulted in a considerable downregulation of HIF-1α, VEGF, MMP2, and MMP9 mRNA and protein expression levels in HOS cells.
"highlight2" >VEGF↓,

3352- QC,    A review of quercetin: Antioxidant and anticancer properties
- Review, Var, NA
"highlight2" >*antiOx↑, Quercetin is considered to be a strong antioxidant due to its ability to scavenge free radicals and bind transition metal ions. T
"highlight2" >*lipid-P↓, properties of quercetin allow it to inhibit lipid peroxidation
"highlight2" >*TNF-α↓, Quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner
"highlight2" >*NF-kB↓, inhibiting the activation of NF-κβ,
"highlight2" >*COX2↓, Quercetin also inhibits the enzymes cyclooxygenase
"highlight2" >*IronCh↑, Quercetin also chelates ions of transition metals such as iron which can initiate the formation of oxygen free radicals
"highlight2" >P53↓, Quercetin (248 microM) was found to down regulate expression of mutant p53 protein to nearly undetectable levels in human breast cancer cell lines.
"highlight2" >TumCCA↑, Quercetin has been found to arrest human leukemic T-cells in the late G1 phase of the cell cycle.
"highlight2" >HSPs↓, Quercetin has been found to inhibit production of heat shock proteins in several malignant cell lines, including breast cancer,[52] leukemia,[53] and colon cancer.[
"highlight2" >P21↓, Quercetin (10 microM) has been found to inhibit the expression of the p21-ras oncogene in cultured colon cancer cell lines
"highlight2" >RAS↓,
"highlight2" >ER(estro)↑, Quercetin has been shown to induce ER II expression in both type I estrogen receptor positive (ER+) and type I estrogen receptor negative (ER-) human breast cancer cells
"highlight2" >OS?, Animals treated daily with 40 mg/kg quercetin had a 20-percent increase in life span, while those treated with 160 mg/kg rutin had a 50% increase in life span.

3351- QC,    Quercetin Exerts Differential Neuroprotective Effects Against H2O2 and Aβ Aggregates in Hippocampal Neurons: the Role of Mitochondria
- Review, AD, NA
"highlight2" >*ROS↓, quercetin decreased ROS levels, recovered the normal morphology of mitochondria, and prevented mitochondrial dysfunction in neurons that were treated with H2O2.
"highlight2" >*neuroP↑, quercetin exerts differential effects on the prevention of H2O2- and Aβ-induced neurotoxicity in hippocampal neurons

3350- QC,    Quercetin and the mitochondria: A mechanistic view
- Review, NA, NA
"highlight2" >*antiOx↑, antioxidant and anti-inflammatory properties
"highlight2" >*Inflam↓,
"highlight2" >*NRF2↑, Quercetin is able to activate the master regulator nuclear factor erythroid 2-related factor 2 (Nrf2)
"highlight2" >ROS⇅, That is, as a free radical-scavenging antioxidant, quercetin protects cells against DNA damage induced by reactiveoxygen species (ROS), but the oxidized quercetin intermediates (see above) can then react with glutathione (GSH) thereby lowering GSH
"highlight2" >*NRF2↑, 10uM (24 h) Mouse primary hepatocytes Activation of Nrf2; ↑HO-1 levels; ↑expression of PPARα and PGC-1α
"highlight2" >*HO-1↑,
"highlight2" >*PPARα↑,
"highlight2" >*PGC-1α↑,
"highlight2" >*SIRT1↑, Rat hippocampus ↑ SIRT1, PGC-1α, NRF-1, and TFAM levels; ATP levels;
"highlight2" >*ATP↑,
"highlight2" >ATP↓, L1210 and P388 leukemia cells (Suolinna et al., 1975). At least in part, the authors attributed the pro-apoptotic effect of quercetin in these cell lines to its capacity to inhibit ATP synthase, causing a decrease in ATP content.
"highlight2" >ERK↓, downregulation of ERK1/2 by quercetin (50-100 uM for 24 or 48 h, combined or not with resveratrol
"highlight2" >cl‑PARP↑, NCaP cells ↑PARP cleavage ↑ Caspase-9, caspase-8, and caspase-3 activities
"highlight2" >Casp9↑,
"highlight2" >Casp8↑,
"highlight2" >BAX↑, MDA-MB-231 cells ↑Bax levels, ↓MMP, ↑cytochrome c release, ↑caspase-9 and caspase-3 activities
"highlight2" >MMP↓,
"highlight2" >Cyt‑c↑,
"highlight2" >Casp3↑,
"highlight2" >HSP27↓, T98G cells: ↓Hsp27 and Hsp72 contents, ↓Ras and Raf level
"highlight2" >HSP72↓,
"highlight2" >RAS↓,
"highlight2" >Raf↓,

3374- QC,    Therapeutic effects of quercetin in oral cancer therapy: a systematic review of preclinical evidence focused on oxidative damage, apoptosis and anti-metastasis
- Review, Oral, NA - Review, AD, NA
"highlight2" >α-SMA↓, In oral cancer cells, quercetin could inhibit EMT via up-regulation of claudin-1 and E-cadherin and down-regulation of α-SMA, vimentin, fibronectin, and Slug [29]
"highlight2" >α-SMA↑, OSC20 Invasion: ↓Migration, ↑Expression of epithelial markers (E-cadherin & claudin-1), ↑Expression of mesenchymal markers (fibronectin, vimentin, & α-SMA),
"highlight2" >TumCP↓, quercetin significantly reduced cancer cell proliferation, cell viability, tumor volume, invasion, metastasis and migration
"highlight2" >tumCV↓,
"highlight2" >TumVol↓,
"highlight2" >TumCI↓,
"highlight2" >TumMeta↓,
"highlight2" >TumCMig↓,
"highlight2" >ROS↑, This anti-cancer agent induced oxidative stress and apoptosis in the cancer cells.
"highlight2" >Apoptosis↑,
"highlight2" >BioAv↓, The efficacy of quercetin (as lipophilic) is much impacted by its poor absorption rates, which define its bioavailability. The research on quercetin's bioavailability in animal models shows it may be as low as 10%
"highlight2" >*neuroP↑, quercetin has been observed to exhibit neuroprotective effects in Alzheimer's disease through its anti-oxidants, and anti-inflammatory properties and inhibition of amyloid-β (Aβ) fibril formation
"highlight2" >*antiOx↑,
"highlight2" >*Inflam↓,
"highlight2" >*Aβ↓,
"highlight2" >*cardioP↑, Additionally, quercetin protects the heart by stopping oxidative stress, inflammation, apoptosis, and protein kinases
"highlight2" >MMP↓, ↓MMP, ↑Cytosolic Cyt. C,
"highlight2" >Cyt‑c↑,
"highlight2" >MMP2↓, ↓Activation MMP-2 & MMP-9, ↓Expression levels of EMT inducers & MMPs, Downregulated Twist & Slug
"highlight2" >MMP9↓,
"highlight2" >EMT↓,
"highlight2" >MMPs↓,
"highlight2" >Twist↓,
"highlight2" >Slug↓,
"highlight2" >Ca+2↑, ↑Apoptosis, ↑ROS, ↑Ca2+ production, ↑Activities of caspase‑3, caspase‑8 & caspase‑9
"highlight2" >AIF↑, ↑Mitochondrial release of Cyt. C, AIF, & Endo G
"highlight2" >Endon↑,
"highlight2" >P-gp↓, ↓ Protein levels of P-gp, & P-gp Expression
"highlight2" >LDH↑, ↑LDH release
"highlight2" >HK2↓, CAL27 cells) 80µM/24h Molecular markers: ↓Activities of HK, PK, & LDH, ↓Glycolysis, ↓Glucose uptake, ↓Lactate production, ↓Viability, ↓G3BP1, & YWHA2 protein levels
"highlight2" >PKA↓,
"highlight2" >Glycolysis↓,
"highlight2" >GlucoseCon↓,
"highlight2" >lactateProd↓,
"highlight2" >GRP78/BiP↑, Quercetin controls the activation of intracellular Ca2+ and calpain-1, which then activates GRP78, caspase-12, and C/EBP homologous protein (CHOP) in oral cancer cells
"highlight2" >Casp12↑,
"highlight2" >CHOP↑,

3348- QC,    Quercetin and iron metabolism: What we know and what we need to know
- Review, NA, NA
"highlight2" >*IronCh↑, Quercetin alleviates iron overload induced by various pathologies as a natural iron chelator.
"highlight2" >*ROS↓, Quercetin's iron-chelating property and direct scavenging action against ROS (reactive oxygen species) are believed to be the essence of its antioxidant activity.
"highlight2" >*AntiAg↑,
"highlight2" >*Fenton↓, Cheng and Breen (Cheng and Breen, 2000) found that quercetin suppressed the Fenton reaction by forming a Fe-quercetin-ATP complex.
"highlight2" >*lipid-P↓, quercetin effectively decreases iron deposition, and it alleviates lipid peroxidation as well as protein oxidation in the livers, kidneys and hearts of iron-dextran-overloaded mice.
"highlight2" >*hepatoP↑, quercetin acts as a reliable liver protector to prevent iron-provoked oxidative damage
"highlight2" >*RenoP↑, modulation of iron by quercetin has been shown to prevent glycerol-induced acute myoglobinuric renal failure
"highlight2" >HIF-1↑, in both human prostate adenocarcinoma cell lines (LNCaP, DU-145, and PC-3 cell lines) and HeLa cells, quercetin treatment appears to induce HIF-1/2αaccumulation, which may give rise to some undesirable consequences in cases such as cancer treatment
"highlight2" >ROS↑, The redox status of quercetin determines whether it can undergo oxido-reductive activation and then be subjected to the iron-involved redox cycling of the Fenton reaction to produce substantial amounts of ROS.

3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
"highlight2" >*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
"highlight2" >*ROS↓,
"highlight2" >*Inflam↓, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
"highlight2" >TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
"highlight2" >Apoptosis↑,
"highlight2" >*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
"highlight2" >*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
"highlight2" >TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
"highlight2" >MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
"highlight2" >NADPH↓,
"highlight2" >ChemoSen↑,
"highlight2" >MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
"highlight2" >TIMP2↑,
"highlight2" >*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
"highlight2" >*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
"highlight2" >*COX2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
"highlight2" >*NF-kB↓,
"highlight2" >*MAPK↓,
"highlight2" >*CRP↓,
"highlight2" >*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
"highlight2" >*TNF-α↓,
"highlight2" >*IL1β↓,
"highlight2" >*TLR4↑,
"highlight2" >*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
"highlight2" >*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
"highlight2" >*ICAM-1↓,
"highlight2" >*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
"highlight2" >*HO-1↑,
"highlight2" >*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
"highlight2" >*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
"highlight2" >*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
"highlight2" >*memory↑, Both memory and learning abilities in the test animals increased
"highlight2" >*cognitive↑,
"highlight2" >*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
"highlight2" >*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
"highlight2" >*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
"highlight2" >*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
"highlight2" >*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
"highlight2" >*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

3346- QC,    Regulation of the Intracellular ROS Level Is Critical for the Antiproliferative Effect of Quercetin in the Hepatocellular Carcinoma Cell Line HepG2
- in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
"highlight2" >TumCCA↑, can induce the cell cycle arrest and apoptosis of hepatocellular carcinoma (HCC) cells by the stabilization or induction of p53
"highlight2" >Apoptosis↑,
"highlight2" >P53↑,
"highlight2" >TumCP↓, quercetin reduced the proliferation of HepG2 cells significantly, but not Huh7 cells
"highlight2" >ROS↓, Interestingly, it was found that quercetin down-regulated the intracellular ROS level of HepG2 cells, but not that of Huh7 cells.
"highlight2" >antiOx↑, quercetin is useful for HCC treatment as an antioxidant.
"highlight2" >HO-1↑, The expression of p53 and HO-1 was upregulated by quercetin after 12 and 24 h, respectively.
"highlight2" >CDK1↓, The expression of p53 and HO-1 was increased but that of CHK1 was decreased in response to the increase in quercetin up to 100 μM.

3344- QC,    Quercetin induced ROS production triggers mitochondrial cell death of human embryonic stem cells
- in-vitro, Nor, hESC
"highlight2" >mt-ROS↑, mitochondrial reactive oxygen species (ROS), strongly induced by QC in human embryonic stem cells (hESCs) but not in human dermal fibroblasts (hDFs), were responsible for QC-mediated hESC’s cell death.
"highlight2" >selectivity↑,
"highlight2" >P53↑, . Increased p53 protein stability and subsequent mitochondrial localization by QC treatment triggered mitochondrial cell death only in hESCs.
"highlight2" >ROS⇅, QC acts either as a pro-oxidant to be cytotoxic to cancer cells with active proliferation [8, 10] or as an anti-oxidant [9], depending on the cell models,

3343- QC,    Quercetin, a Flavonoid with Great Pharmacological Capacity
- Review, Var, NA - Review, AD, NA - Review, Arthritis, NA
"highlight2" >*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
"highlight2" >*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
"highlight2" >*angioG↓,
"highlight2" >*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
"highlight2" >*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
"highlight2" >*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
"highlight2" >*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
"highlight2" >*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
"highlight2" >*Catalase↑,
"highlight2" >*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
"highlight2" >*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
"highlight2" >*cardioP↑, quercetin has positive effects on cardiovascular diseases
"highlight2" >*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
"highlight2" >*TNF-α↓,
"highlight2" >*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
"highlight2" >*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
"highlight2" >*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
"highlight2" >*neuroP↑,
"highlight2" >*Pain↓, quercetin reduces pain and inflammation associated with arthritis
"highlight2" >*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
"highlight2" >*NRF2↑,
"highlight2" >*HO-1↑,
"highlight2" >*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
"highlight2" >*IL17↓,
"highlight2" >*MCP1↓,
"highlight2" >PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
"highlight2" >ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
"highlight2" >BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
"highlight2" >cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
"highlight2" >KRAS↓,
"highlight2" >ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
"highlight2" >selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
"highlight2" >tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
"highlight2" >Apoptosis↑,
"highlight2" >TumCCA↑,
"highlight2" >eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
"highlight2" >P-gp↓,
"highlight2" >eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
"highlight2" >eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
"highlight2" >eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
"highlight2" >eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
"highlight2" >CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
"highlight2" >CDK1↓,
"highlight2" >CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
"highlight2" >CDK2↓,
"highlight2" >TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
"highlight2" >Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
"highlight2" >cl‑PARP↑,
"highlight2" >MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
"highlight2" >HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
"highlight2" >HSP90↓,
"highlight2" >MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
"highlight2" >RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
"highlight2" >eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

3342- QC,    Quercetin modulates OTA-induced oxidative stress and redox signalling in HepG2 cells — up regulation of Nrf2 expression and down regulation of NF-κB and COX-2
- in-vitro, Nor, HepG2
"highlight2" >*ROS↓, Pre-treatment with quercetin ameliorated ROS and calcium release as well as NF-κB induction and expression
"highlight2" >*Ca+2↓,
"highlight2" >*NF-kB↓,
"highlight2" >*NRF2↑, Quercetin induced Nrf-2 nuclear translocation and expression.
"highlight2" >*COX2↓, Quercetin's anti-inflammatory property was exhibited as it down regulated COX-2.
"highlight2" >*Inflam↓,

3341- QC,    Antioxidant Activities of Quercetin and Its Complexes for Medicinal Application
- Review, Var, NA - Review, Stroke, NA
"highlight2" >*antiOx↑, we highlight the recent advances in the antioxidant activities, chemical research, and medicinal application of quercetin.
"highlight2" >*BioAv↑, Moreover, owing to its high solubility and bioavailability,
"highlight2" >*GSH↑, Animal and cell studies found that quercetin induces GSH synthesis
"highlight2" >*AChE↓, In this way, it has a stronger inhibitory effect against key enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), which are associated with oxidative properties
"highlight2" >*BChE↓,
"highlight2" >*H2O2↓, Quercetin has been shown to alleviate the decline of manganese-induced antioxidant enzyme activity, the increase of AChE activity, hydrogen peroxide generation, and lipid peroxidation levels in rats, thereby preventing manganese poisoning
"highlight2" >*lipid-P↓,
"highlight2" >*SOD↑, quercetin significantly enhanced the expression levels of endogenous antioxidant enzymes such as Cu/Zn SOD, Mn SOD, catalase (CAT), and GSH peroxidase in the hippocampal CA1 pyramidal neurons of animals suffering from ischemic injury.
"highlight2" >*SOD2↑,
"highlight2" >*Catalase↑,
"highlight2" >*GPx↑,
"highlight2" >*neuroP↑, Thus, quercetin may be a potential neuroprotective agent for transient ischemia
"highlight2" >*HO-1↑, quercetin can promote fracture healing in smokers by removing free radicals and upregulating the expression of heme-oxygenase- (HO-) 1 and superoxide-dismutase- (SOD-) 1, which protects primary human osteoblasts exposed to cigarette smoke
"highlight2" >*cardioP↑, Quercetin has also been shown to prevent heart damage by clearing oxygen-free radicals caused by lipopolysaccharide (LPS)-induced endotoxemia.
"highlight2" >*MDA↓, quercetin treatment increased the levels of SOD and CAT and reduced the level of MDA after LPS induction, suggesting that quercetin enhanced the antioxidant defense system
"highlight2" >*NF-kB↓, quercetin promotes disease recovery by downregulating the expression of NIK and NF-κB including IKK and RelB, and upregulating the expression of TRAF3.
"highlight2" >*IKKα↓,
"highlight2" >*ROS↓, quercetin controls the development of atherosclerosis induced by a high-fructose diet by inhibiting ROS and enhancing PI3K/AKT.
"highlight2" >*PI3K↑,
"highlight2" >*Akt↑,
"highlight2" >*hepatoP↑, Quercetin exerts antioxidant and hepatoprotective effects against acute liver injury in mice induced by tertiary butyl hydrogen peroxide. T
"highlight2" >P53↑, Quercetin prevents cancer development by upregulating p53, which is the most common inactivated tumor suppressor. It also increases the expression of BAX, a downstream target of p53 and a key pro-apoptotic gene in HepG2 cells
"highlight2" >BAX↑,
"highlight2" >IGF-1R↓, Studies have found that insulin-like growth factor receptor 1 (IGFIR), AKT, androgen receptor (AR), and cell proliferation and anti-apoptotic proteins are increased in cancer, but quercetin supplementation normalizes their expression
"highlight2" >Akt↓,
"highlight2" >AR↓,
"highlight2" >TumCP↓,
"highlight2" >GSH↑, Moreover, quercetin significantly increases antioxidant enzyme levels, including GSH, SOD, and CAT, and inhibits lipid peroxides, thereby preventing skin cancer induced by 7,12-dimethyl Benz
"highlight2" >SOD↑,
"highlight2" >Catalase↑,
"highlight2" >lipid-P↓,
"highlight2" >*TNF-α↓, Heart: increases TNF-α, and prevents Ca2+ overload-induced myocardial cell injury
"highlight2" >*Ca+2↓,

3340- QC,    Quercetin regulates inflammation, oxidative stress, apoptosis, and mitochondrial structure and function in H9C2 cells by promoting PVT1 expression
- in-vitro, Nor, H9c2
"highlight2" >*Inflam↓, Quercetin promotes the proliferation of H9C2 cells, while inhibiting inflammation, oxidative stress, and cell apoptosis, and alleviating the structural and functional dysfunction of mitochondria.
"highlight2" >*ROS↓,
"highlight2" >*Apoptosis↓,

3366- QC,    Quercetin Attenuates Endoplasmic Reticulum Stress and Apoptosis in TNBS-Induced Colitis by Inhibiting the Glucose Regulatory Protein 78 Activation
- in-vivo, IBD, NA
"highlight2" >*Apoptosis↓, quercetin improved TNBS-induced histopathological alterations, apoptosis, inflammation, oxidative stress, and ER stress
"highlight2" >*Inflam↓,
"highlight2" >*ROS↓,
"highlight2" >*ER Stress↓, suggests that quercetin has a regulatory effect on ER stress-mediated apoptosis, and thus may be beneficial in treating IBD.
"highlight2" >*TNF-α↓, Quercetin reduced the TNF-α and MPO levels associated with colitis
"highlight2" >*MPO↓,
"highlight2" >*p‑JNK↓, The HSCORE values of p-JNK (p < 0.001), caspase-12 (p < 0.001), and GRP78 (p = 0.004) were lowered in the quercetin group when compared to the colitis group
"highlight2" >*Casp12↓,
"highlight2" >*GRP78/BiP↓,
"highlight2" >*antiOx↑, protective effect of quercetin in IBD, attributed to its antioxidant properties and NF-kB inhibition
"highlight2" >*NF-kB↓,

3375- QC,    Quercetin Mediated TET1 Expression Through MicroRNA-17 Induced Cell Apoptosis in Melanoma Cells
- in-vitro, Melanoma, B16-BL6
"highlight2" >TET1↑, Our results suggest that the expression of TET1 was increased following treatment with quercetin in OCM-1, SK-MEL-1, and B16 cells.
"highlight2" >TumCI↓, The results showed that the increased expression of TET1-induced apoptosis, increased 5-hydroxymethylcytosine (5 hmC). and inhibited invasion.

3373- QC,    The Effect of Quercetin in the Yishen Tongluo Jiedu Recipe on the Development of Prostate Cancer through the Akt1-related CXCL12/ CXCR4 Pathway
- in-vitro, Pca, DU145
"highlight2" >TumCP↓, Quercetin inhibited the proliferation of DU145 cells by upregulating caspase-3 and downregulating Bcl-2 expression, promoting apoptosis and reducing invasion and migration abilities.
"highlight2" >Casp3↑,
"highlight2" >Bcl-2↓,
"highlight2" >Apoptosis↑,
"highlight2" >TumCI↓,
"highlight2" >TumCMig↓,
"highlight2" >CXCL12↓, In vivo, quercetin downregulated CXCL12 and CXCR4 expressions and inhibited PCa development by the Akt1-related CXCL12/CXCR4 pathway.
"highlight2" >CXCR4↓,

3372- QC,  FIS,  KaempF,    Anticancer Potential of Selected Flavonols: Fisetin, Kaempferol, and Quercetin on Head and Neck Cancers
- Review, HNSCC, NA
"highlight2" >ROCK1↑, quercetin affects the level of RhoA and NF-κB proteins in SAS cells, and stimulates the expression of RhoA, ROCK1, and NF-κB in SAS cells [53].
"highlight2" >TumCCA↓, inhibition of the cell cycle;
"highlight2" >HSPs↓, inhibition of heat shock proteins;
"highlight2" >RAS↓, inhibition of Ras protein expression.
"highlight2" >ROS↑, fisetin induces production of reactive oxygen species (ROS), increases Ca2+ release, and decreases the mitochondrial membrane potential (Ψm) in head and neck neoplastic cells.
"highlight2" >Ca+2↑,
"highlight2" >MMP↓,
"highlight2" >Cyt‑c↑, quercetin increases the expression level of cytochrome c, apoptosis inducing factor and endonuclease G
"highlight2" >Endon↑,
"highlight2" >MMP9↓, quercetin inhibits MMP-9 and MMP-2 expression and reduces levels of the following proteins: MMP-2, -7, -9 [49,53] and -10
"highlight2" >MMP2↓,
"highlight2" >MMP7↓,
"highlight2" >MMP-10↓,
"highlight2" >VEGF↓, as well as VEGF, NF-κB p65, iNOS, COX-2, and uPA, PI3K, IKB-α, IKB-α/β, p-IKKα/β, FAK, SOS1, GRB2, MEKK3 and MEKK7, ERK1/2, p-ERK1/2, JNK1/2, p38, p-p38, c-JUN, and pc-JUN
"highlight2" >NF-kB↓,
"highlight2" >p65↓,
"highlight2" >iNOS↓,
"highlight2" >COX2↓,
"highlight2" >uPA↓,
"highlight2" >PI3K↓,
"highlight2" >FAK↓,
"highlight2" >MEK↓,
"highlight2" >ERK↓,
"highlight2" >JNK↓,
"highlight2" >p38↓,
"highlight2" >cJun↓,
"highlight2" >FOXO3↑, Quercetin causes an increase in the level of FOXO1 protein both in a dose- and time-dependent way; however, it does not affect changes in expression of FOXO3a

3371- QC,    Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways
- in-vitro, GBM, T98G
"highlight2" >TIMP2↑, MMP2, and MMP9 was significantly decreased by quercetin treatment, while TIMP1 and TIMP2 were upregulated (
"highlight2" >TumCG↓, Quercetin significantly suppressed the growth and migration of human GBM T98G cells, induced apoptosis, and arrested cells in the S-phase cell cycle
"highlight2" >TumCMig↓,
"highlight2" >Apoptosis↑,
"highlight2" >TumCCA↑,
"highlight2" >MMP↓, collapse of mitochondrial membrane potential, ROS generation, enhanced Bax/Bcl-2 ratio, and strengthened cleaved-Caspase 9 and cleaved-Caspase 3 suggested the involvement of ROS-mediated mitochondria-dependent apoptosis in the process
"highlight2" >ROS↑,
"highlight2" >Bax:Bcl2↑,
"highlight2" >cl‑Casp9↑,
"highlight2" >cl‑Casp3↑,
"highlight2" >DNAdam↑, quercetin-induced apoptosis was accompanied by intense DNA double-strand breaks (DSBs), γH2AX foci formation, methylation of MGMT promoter, increased cleaved-PARP, and reduced MGMT expression
"highlight2" >γH2AX↑,
"highlight2" >MGMT↓,
"highlight2" >cl‑PARP↑,

3370- QC,    Quercetin downregulates matrix metalloproteinases 2 and 9 proteins expression in prostate cancer cells (PC-3)
- in-vitro, Pca, PC3
"highlight2" >MMP2↓, quercetin treatment decreased the expressions of MMP-2 and MMP-9 in dose-dependent manner.
"highlight2" >MMP9↓,

3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
"highlight2" >FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
"highlight2" >TumCCA↑, stimulation of cell cycle arrest at the G1 stage
"highlight2" >p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
"highlight2" >CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
"highlight2" >CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
"highlight2" >CDK1↓,
"highlight2" >EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
"highlight2" >PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
"highlight2" >MAPK↓,
"highlight2" >Wnt↓,
"highlight2" >ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
"highlight2" >miR-21↑,
"highlight2" >Akt↓, Figure 1 anti-cancer mechanisms
"highlight2" >NF-kB↓,
"highlight2" >FasL↑,
"highlight2" >Bak↑,
"highlight2" >BAX↑,
"highlight2" >Bcl-2↓,
"highlight2" >Casp3↓,
"highlight2" >Casp9↑,
"highlight2" >P53↑,
"highlight2" >p38↑,
"highlight2" >MAPK↑,
"highlight2" >Cyt‑c↑,
"highlight2" >PARP↓,
"highlight2" >CHOP↑,
"highlight2" >ROS↓,
"highlight2" >LDH↑,
"highlight2" >GRP78/BiP↑,
"highlight2" >ERK↑,
"highlight2" >MDA↓,
"highlight2" >SOD↑,
"highlight2" >GSH↑,
"highlight2" >NRF2↑,
"highlight2" >VEGF↓,
"highlight2" >PDGF↓,
"highlight2" >EGF↓,
"highlight2" >FGF↓,
"highlight2" >TNF-α↓,
"highlight2" >TGF-β↓,
"highlight2" >VEGFR2↓,
"highlight2" >EGFR↓,
"highlight2" >FGFR1↓,
"highlight2" >mTOR↓,
"highlight2" >cMyc↓,
"highlight2" >MMPs↓,
"highlight2" >LC3B-II↑,
"highlight2" >Beclin-1↑,
"highlight2" >IL1β↓,
"highlight2" >CRP↓,
"highlight2" >IL10↓,
"highlight2" >COX2↓,
"highlight2" >IL6↓,
"highlight2" >TLR4↓,
"highlight2" >Shh↓,
"highlight2" >HER2/EBBR2↓,
"highlight2" >NOTCH↓,
"highlight2" >DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
"highlight2" >HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
"highlight2" >CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
"highlight2" >angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
"highlight2" >uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
"highlight2" >uPAR↓,
"highlight2" >RAS↓,
"highlight2" >Raf↓,
"highlight2" >TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis

3368- QC,    The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update
- Review, Var, NA
"highlight2" >*Inflam↓, quercetin is known for its anti-inflammatory, antioxidant, and anticancer properties.
"highlight2" >*antiOx↑,
"highlight2" >*AntiCan↑,
"highlight2" >Casp3↓, Quercetin increases apoptosis and autophagy in cancer by activating caspase-3, inhibiting the phosphorylation of Akt, mTOR, and ERK, lessening β-catenin, and stabilizing the stabilization of HIF-1α.
"highlight2" >p‑Akt↓,
"highlight2" >p‑mTOR↓,
"highlight2" >p‑ERK↓,
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >Hif1a↓,
"highlight2" >AntiAg↓, Quercetin have revealed an anti-tumor effect by reducing development of blood vessels. I
"highlight2" >VEGFR2↓, decrease tumor growth through targeting VEGFR-2-mediated angiogenesis pathway and suppressing the downstream regulatory component AKT in prostate and breast malignancies.
"highlight2" >EMT↓, effects of quercetin on inhibition of EMT, angiogenesis, and invasiveness through the epidermal growth factor receptor (EGFR)/VEGFR-2-mediated pathway in breast cancer
"highlight2" >EGFR↓,
"highlight2" >MMP2↓, MMP2 and MMP9 are two remarkable compounds in metastatic breast cancer (28–30). quercetin on breast cancer cell lines (MDA-MB-231) and showed that after treatment with this flavonoid, the expression of these two proteinases decreased
"highlight2" >MMP↓,
"highlight2" >TumMeta↓, head and neck (HNSCC), the inhibitory effect of quercetin on the migration of tumor cells has been shown by regulating the expression of MMPs
"highlight2" >MMPs↓,
"highlight2" >Akt↓, quercetin by inhibiting the Akt activation pathway dependent on Snail, diminishing the expression of N-cadherin, vimentin, and ADAM9 and raising the expression of E-cadherin and proteins
"highlight2" >Snail↓,
"highlight2" >N-cadherin↓,
"highlight2" >Vim↓,
"highlight2" >E-cadherin↑,
"highlight2" >STAT3↓, inhibiting STAT3 signaling
"highlight2" >TGF-β↓, reducing the expression of TGF-β caused by vimentin and N-cadherin, Twist, Snail, and Slug and increasing the expression of E-cadherin in PC-3 cells.
"highlight2" >ROS↓, quercetin exerted an anti-proliferative role on HCC cells by lessening intracellular ROS independently of p53 expression
"highlight2" >P53↑, increasing the expression of p53 and BAX in hepatocellular carcinoma (HepG2) cell lines through the reduction of PKC, PI3K, and cyclooxygenase (COX-2)
"highlight2" >BAX↑,
"highlight2" >PKCδ↓,
"highlight2" >PI3K↓,
"highlight2" >COX2↓,
"highlight2" >cFLIP↓, quercetin by inhibiting PI3K/AKT/mTOR and STAT3 pathways, decreasing the expression of cellular proteins such as c-FLIP, cyclin D1, and c-Myc, as well as reducing the production of IL-6 and IL-10 cytokines, leads to the death of PEL cells
"highlight2" >cycD1/CCND1↓,
"highlight2" >cMyc↓,
"highlight2" >IL6↓,
"highlight2" >IL10↓,
"highlight2" >Cyt‑c↑, In addition, quercetin induced c-cytochrome-dependent apoptosis and caspase-3 almost exclusively in the HSB2 cell line
"highlight2" >TumCCA↑, Exposure of K562 cells to quercetin also significantly raised the cells in the G2/M phase, which reached a maximum peak in 24 hours
"highlight2" >DNMTs↓, pathway through DNA demethylation activity, histone deacetylase (HDAC) repression, and H3ac and H4ac enrichment
"highlight2" >HDAC↓,
"highlight2" >ac‑H3↑,
"highlight2" >ac‑H4↑,
"highlight2" >Diablo↑, SMAC/DIABLO exhibited activation
"highlight2" >Casp3↑, enhanced levels of activated caspase 3, cleaved caspase 9, and PARP1
"highlight2" >Casp9↑,
"highlight2" >PARP1↑,
"highlight2" >eff↑, green tea and quercetin as monotherapy caused the reduction of levels of anti-apoptotic proteins, CDK6, CDK2, CYCLIN D/E/A, BCL-2, BCL-XL, and MCL-1 and an increase in expression of BAX.
"highlight2" >PTEN↑, Quercetin upregulates the level of PTEN as a tumor suppressor, which inhibits AKT signaling
"highlight2" >VEGF↓, Quercetin had anti-inflammatory and anti-angiogenesis effects, decreasing VGEF-A, NO, iNOS, and COX-2 levels
"highlight2" >NO↓,
"highlight2" >iNOS↓,
"highlight2" >ChemoSen↑, quercetin and chemotherapy can potentiate their effect on the malignant cell
"highlight2" >eff↑, combination with hyperthermia, Shen et al. Quercetin is a method used in cancer treatment by heating, and it was found to reduce Doxorubicin hydrochloride resistance in leukemia cell line K562
"highlight2" >eff↑, treatment with ellagic acid, luteolin, and curcumin alone showed excellent anticancer effects.
"highlight2" >eff↑, co-treatment with quercetin and curcumin led to a reduction of mitochondrial membrane integrity, promotion of cytochrome C release, and apoptosis induction in CML cells
"highlight2" >uPA↓, A-549 cells were shown to have reduced mRNA expressions of urokinase plasminogen activator (uPA), Upar, protein expression of CXCR-4, CXCL-12, SDF-1 when quercetin was applied at 20 and 40 mM/ml by real-time PCR.
"highlight2" >CXCR4↓,
"highlight2" >CXCL12↓,
"highlight2" >CLDN2↓, A-549 cells, indicated that quercetin could reduce mRNA and protein expression of Claudin-2 in A-549 cell lines without involving Akt and ERK1/2,
"highlight2" >CDK6↓, CDK6, which supports the growth and viability of various cancer cells, was hampered by the dose-dependent manner of quercetin (IC50 dose of QR for A-549 cells is 52.35 ± 2.44 μM).
"highlight2" >MMP9↓, quercetin up-regulated the rates of G1 phase cell cycle and cellular apoptotic in both examined cell lines compared with the control group, while it declined the expressions of the PI3K, AKT, MMP-2, and MMP-9 proteins
"highlight2" >TSP-1↑, quercetin increased TSP-1 mRNA and protein expression to inhibit angiogenesis,
"highlight2" >Ki-67↓, significant reductions in Ki67 and PCNA proliferation markers and cell survival markers in response to quercetin and/or resveratrol.
"highlight2" >PCNA↓,
"highlight2" >ROS↑, Also, quercetin effectively causes intracellular ROS production and ER stress
"highlight2" >ER Stress↑,

3367- QC,    Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments
- Review, Stroke, NA - Review, AD, NA
"highlight2" >*NRF2↑, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus.
"highlight2" >*neuroP↑,
"highlight2" >*motorD↑, Que protected the blood-brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction.
"highlight2" >*Inflam↓, (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex
"highlight2" >*cognitive↑, (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1-4, antioxidant activity, and Nrf2 levels in the brain.

3365- QC,    Quercetin attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of SIRT1/AMPK pathways
- in-vivo, Sepsis, NA
"highlight2" >*ER Stress↓, quercetin could inhibit the level of ER stress as evidenced by decreased mRNA expression of PDI, CHOP, GRP78, ATF6, PERK, IRE1α
"highlight2" >*PDI↓,
"highlight2" >*CHOP↓,
"highlight2" >*GRP78/BiP↓,
"highlight2" >*ATF6↓,
"highlight2" >*PERK↓,
"highlight2" >*IRE1↓,
"highlight2" >*MMP↑, and improve mitochondrial function, as presented by increased MMP, SOD level and reduced production of ROS, MDA.
"highlight2" >*SOD↑,
"highlight2" >*ROS↓,
"highlight2" >*MDA↓,
"highlight2" >*SIRT1↑, quercetin upregulated SIRT1/AMPK mRNA expression.
"highlight2" >*AMPK↑,
"highlight2" >*Sepsis↓, quercetin could protect against sepsis-induced ALI by suppressing oxidative stress-mediated ER stress and mitochondrial dysfunction via induction of the SIRT1/AMPK pathways.

3364- QC,    Quercetin Protects Human Thyroid Cells against Cadmium Toxicity
- in-vitro, Nor, NA
"highlight2" >*MDA↓, MDA production was increased significantly after incubation with CdCl 2 1 and 10 μM compared with untreated cells (p < 0.001). This effect was significantly attenuated when the cultures were supple‐ mented with quercetin
"highlight2" >*GRP78/BiP↓, A significant increase in GRP78 protein expression was detected in Nthy‐ori‐3‐1 cells exposed to 0.1 or 1 μM of CdCl 2 for 2 h compared with untreated cells. Again, this action was reversed by pretreatment with quercetin 5 μM

3363- QC,    The Protective Effect of Quercetin on Endothelial Cells Injured by Hypoxia and Reoxygenation
- in-vitro, Nor, HBMECs
"highlight2" >*Apoptosis↓, Quercetin can promote the viability, migration and angiogenesis of HBMECs, and inhibit the apoptosis.
"highlight2" >*angioG↑,
"highlight2" >*NRF2↑, quercetin can also activate Keap1/Nrf2 signaling pathway, reduce ATF6/GRP78 protein expression.
"highlight2" >*Keap1↓,
"highlight2" >*ATF6↓,
"highlight2" >*GRP78/BiP↓,
"highlight2" >*CLDN5↑, quercetin could increase the expression of Claudin-5 and Zonula occludens-1.
"highlight2" >*ZO-1↑,
"highlight2" >*MMP↑, reducing mitochondrial membrane potential damage and inhibiting cell apoptosis.
"highlight2" >*BBB↑, quercetin can increase the level of BBB connexin, suggesting that quercetin can maintain BBB integrity.
"highlight2" >*ROS↓, Quercetin Could Inhibit Oxidative Stress
"highlight2" >*ER Stress↓, In our study, ER stress was activated by H/R, and the levels of ATF6 and GRP78 were increased. Quercetin at 1 μmol/L was able to significantly reduce the protein levels of both, inhibit ER stress, and protect HBMECs from H/R injury

3362- QC,    The effect of quercetin on cervical cancer cells as determined by inducing tumor endoplasmic reticulum stress and apoptosis and its mechanism of action
- in-vitro, Cerv, HeLa
"highlight2" >Apoptosis↑, The apoptosis rate in the quercetin group increased significantly in comparison with the blank control group,
"highlight2" >cycD1/CCND1↓, Cyclin D1 showed a tendency to decrease progressively
"highlight2" >Casp3↑, Caspase-3, GRP78, and CHOP expression levels in the quercetin intervention group rose significantly in comparison with the blank control group
"highlight2" >GRP78/BiP↑,
"highlight2" >CHOP↑,
"highlight2" >tumCV↓, viability of the cervical cancer HeLe cells was inhibited by quercetin in a dose-dependent manner
"highlight2" >IRE1↑, The IRE1, p-Perk, and c-ATF6 levels in the quercetin intervention group (20, 40, and 80 μmol/L) rose gradually in comparison with the blank control group
"highlight2" >p‑PERK↑,
"highlight2" >c-ATF6↑,
"highlight2" >ER Stress↑, quercetin can induce ERS to initiate HeLe cell apoptosis.

3361- QC,    Quercetin ameliorates testosterone secretion disorder by inhibiting endoplasmic reticulum stress through the miR-1306-5p/HSD17B7 axis in diabetic rats
- in-vivo, Nor, NA - in-vitro, NA, NA
"highlight2" >*BG↓, Two doses of quercetin increased rat body weight and testicular weight, decreased blood glucose, and inhibited oxidative stress.
"highlight2" >*ROS↓,
"highlight2" >*SOD↑, Both doses of quercetin reduced reactive oxygen species and malondialdehyde levels, and increased superoxide dismutase level in HG-treated cells.
"highlight2" >*MDA↓,
"highlight2" >*ER Stress↓, quercetin inhibits endoplasmic reticulum stress
"highlight2" >*iNOS↓, Quercetin could eliminate the upregulation of iNOS, ET-1, and AR mRNA levels in HG-treated cells
"highlight2" >*CHOP↓, HG treatment increased CHOP and Grp78 mRNA and protein levels in HG-treated cells, and two doses (5 or 10 μM) of quercetin all decreased these levels
"highlight2" >*GRP78/BiP↓,
"highlight2" >*antiOx↓, Quercetin is a natural polyphenol compound with anti-inflammatory [37], anti-oxidant [38], and blood sugar lowering properties
"highlight2" >*Inflam↓,
"highlight2" >*JAK2↑, Our results in vitro showed that quercetin treatment upregulated the phosphorylation levels of JAK2 and STAT3 in HG treated cells. (activating of the JAK2/STAT3 pathway could inhibit ER stress)
"highlight2" >*STAT3?,

3360- QC,    Role of Flavonoids as Epigenetic Modulators in Cancer Prevention and Therapy
- Review, Var, NA
"highlight2" >HDAC↓, Quercetin modulates the expression of various chromatin modifiers and declines the activity of HDACs, DNMTs and HMTs in a dose-dependent manner in human cervical cancer (HeLa) cells
"highlight2" >DNMTs↓,
"highlight2" >HMTs↓,
"highlight2" >Let-7↑, Quercetin also induced let-7c which decreased pancreatic tumor growth by posttranscriptional activation of Numbl and indirect inhibition of Notch
"highlight2" >NOTCH↓,

3359- QC,    Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells
- in-vitro, Cerv, HeLa
"highlight2" >DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
"highlight2" >HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
"highlight2" >HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
"highlight2" >DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
"highlight2" >EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
"highlight2" >HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
"highlight2" >HDAC2↓,
"highlight2" >HDAC6↓,
"highlight2" >HDAC11↓,
"highlight2" >G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
"highlight2" >TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
"highlight2" >PTEN↑,
"highlight2" >SOCS1↑,

3358- QC,    Effects of quercetin on the DNA methylation pattern in tumor therapy: an updated review
- Review, NA, NA
"highlight2" >TET1↑, graphical abstract
"highlight2" >DNMTs↓, Here, we review the structure and properties of quercetin, its capacity for DNA methylation modification in tumors

871- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1
"highlight2" >T-Cell↑, in tumor microenviroment
"highlight2" >Neut↓,
"highlight2" >Macrophages↓,
"highlight2" >ROS↑, RCQ significantly increased reactive oxygen species
"highlight2" >MMP↓, in cancer cells
"highlight2" >other↓, alleviate immunosuppression of the tumor microenvironment to enhance the anti-tumor effect.
"highlight2" >AntiTum↑, at least nearly 5 times higher than that of a single Res/Cur/Que  = 1:1:0.5
"highlight2" >TumVol↓, 35-47% tumor inhibition rate

105- RES,  QC,    The Effect of Resveratrol and Quercetin on Epithelial-Mesenchymal Transition in Pancreatic Cancer Stem Cell
- in-vitro, Pca, PANC1
"highlight2" >N-cadherin↓, Quercetin could prevent Epithelial Mesenchymal Transition by reducing expression of N-cadherin
"highlight2" >TNF-α↓,
"highlight2" >ACTA2↓,
"highlight2" >EMT↓, The reduction in N-cadherin and ACTA-2 immunoreactivities was higher than the increase in vimentin immunoreactivity, quercetin could prevent EMT to a greater extent than resveratrol in pancreatic cancer stem cells because of the reduced expression of
"highlight2" >CD133↓, resveratrol at 5 mM concentration was more effective in reducing both CD133þ and CD133 cell growth when compared with other concentrations for 24-h incubation period
"highlight2" >CSCs↓, Therefore, both quercetin and resveratrol could inhibit EMT of pancreatic cancer stem cell by decreas- ing N-cadherin expression.

104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
"highlight2" >Casp3↑, RQ also induced caspase-3-cleavage (2-fold) and increased PARP cleavage.
"highlight2" >PARP↑,
"highlight2" >survivin↓, RQ also decreased expression of survivin protein
"highlight2" >miR-27a-3p↓, RQ decreased microRNA-27a (miR-27a) and induced zinc finger protein ZBTB10
"highlight2" >Sp1/3/4↓, RQ treatment decreased the expression of Sp1, Sp3, and Sp4 mRNA and this was accompanied by decreased protein expression
"highlight2" >ZBTB10↑,
"highlight2" >ROS⇅, RQ slightly induced the generation of ROS at low concentrations (0–10 μg/mL) whereas at concentrations higher than 20 μg/mL generation of ROS was significantly reduced
"highlight2" >TAC↑, RQ decreased the generation of reactive oxygen species (ROS) by up to 2.25-fold and increased the antioxidant capacity by up to 3-fold in HT-29 cells (3.8-60 μg/mL)
"highlight2" >tumCV↓, HT-29 cell viability (Fig. 2A) was significantly decreased by RQ in a dose- and time-dependent manner

103- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- vitro+vivo, BC, 4T1
"highlight2" >ROS↑, RCQ significantly increased reactive oxygen species (ROS), reduce mitochondrial membrane potentials in cancer cells, and modulate pro-apoptotic Bcl-2 family members
"highlight2" >MMP↓,
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >Casp9↑,
"highlight2" >T-Cell↑, (CD4+CD8+)
"highlight2" >TGF-β↓,

3632- RosA,  CA,  QC,    Evolving Role of Natural Products from Traditional Medicinal Herbs in the Treatment of Alzheimer's Disease
- Review, AD, NA
"highlight2" >*AChE↓, rosmarinic acid, carnosic acid, quercetin, and isorosmanol were isolated from Saliva species, and these constituents also showed the reduction in AChE activity

1309- TQ,  QC,    Thymoquinone and quercetin induce enhanced apoptosis in non-small cell lung cancer in combination through the Bax/Bcl2 cascade
- in-vitro, Lung, NA
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >Apoptosis↑,

114- VitC,  QC,    Chemoprevention of prostate cancer cells by vitamin C plus quercetin: role of Nrf2 in inducing oxidative stress
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
"highlight2" >GPx↓, significant reduction of GPx, GR and NQO1 enzymatic activity
"highlight2" >GSR↓,
"highlight2" >NQO1↓,
"highlight2" >NRF2↓, Our study revealed the significant effects of sequential treatment with VC + Q on Nrf2 suppression in prostate cancer cells
"highlight2" >ROS↑, The level of ROS had significant reduction up to 18% (P ¼ 0.046) when DU145 cells treated with dose no.1 of VC þ Q to compare with the control

3108- VitC,  QC,    The role of quercetin and vitamin C in Nrf2-dependent oxidative stress production in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Lung, A549
"highlight2" >NRF2↓, significant decrease in the expression of Nrf2 mRNA and protein levels following the treatment of breast cancer cells with VC and Q
"highlight2" >HO-1↓, In the MDA-MB 231 and MCF-7 cell lines, HO1 was significantly suppressed following treatment with VC and Q
"highlight2" >ROS↑, It was demonstrated that ROS levels significantly increased in tumor cells treated with VC and Q.
"highlight2" >NRF2⇅, it was demonstrated that treatment of MDA-MB 231 cells with 25 µM Q increased the expression of Nrf2, while 50 and 75 µM Q decreased the mRNA levels of Nrf2.


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 210

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

NA?, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   Ferroptosis↑, 1,   GPx↓, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↓, 9,   GSH↑, 3,   GSH∅, 1,   GSR↓, 1,   GSR↑, 1,   H2O2↓, 1,   H2O2↑, 2,   i-H2O2↓, 1,   HO-1↓, 1,   HO-1↑, 2,   Iron↓, 1,   lipid-P↓, 2,   MDA↓, 1,   NQO1↓, 1,   NQO1↑, 1,   NRF2↓, 5,   NRF2↑, 3,   NRF2⇅, 1,   p‑NRF2↓, 1,   OXPHOS↝, 1,   p66Shc↓, 1,   PrxI∅, 1,   PrxII↑, 1,   PrxII∅, 1,   ROS↓, 8,   ROS↑, 51,   ROS⇅, 9,   ROS∅, 2,   mt-ROS↑, 1,   SOD↑, 4,   TAC↑, 2,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 3,   ATP↓, 3,   ATP↝, 1,   BCR↓, 1,   CDC16↓, 1,   EGF↓, 2,   FGFR1↓, 1,   MEK↓, 1,   p‑MEK↓, 1,   mitResp↓, 1,   MMP↓, 20,   OCR↓, 1,   p‑p42↑, 1,   Raf↓, 4,   XIAP↓, 3,   XIAP↝, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   AKT1↓, 1,   AMACR↓, 1,   AMPK↑, 1,   cMyc↓, 10,   ECAR↓, 1,   FAO↓, 1,   FASN↓, 1,   GlucoseCon↓, 5,   Glycolysis↓, 7,   HK2↓, 6,   lactateProd↓, 7,   LDH↑, 2,   LDHA↓, 3,   NADPH↓, 1,   PDK3↓, 1,   PFKP?, 1,   PI3K/Akt↓, 9,   PI3K/Akt⇅, 1,   PI3k/Akt/mTOR↓, 3,   PKM2↓, 4,   PPARγ↑, 1,   SLC1A5↓, 1,   SREBP1↓, 2,  

Cell Death ⓘ

Akt↓, 17,   p‑Akt↓, 7,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 35,   ASK1↑, 1,   aSmase↝, 1,   BAD↓, 3,   BAD↑, 1,   Bak↑, 1,   BAX↓, 1,   BAX↑, 25,   Bax:Bcl2↑, 4,   Bcl-2↓, 21,   Bcl-2↑, 1,   Bcl-xL↓, 4,   Bcl-xL↑, 1,   BIM↑, 1,   Casp↑, 2,   Casp1↑, 1,   Casp10↑, 3,   Casp12↑, 1,   Casp3↓, 2,   Casp3↑, 29,   cl‑Casp3↑, 2,   Casp7↑, 5,   Casp8↑, 8,   Casp9↑, 18,   cl‑Casp9↑, 2,   CBP↑, 1,   cFLIP↓, 5,   Chk2↑, 1,   CK2↓, 1,   CSR1↑, 1,   Cyt‑c↑, 12,   Diablo↑, 2,   DR4↑, 1,   DR5↓, 1,   DR5↑, 7,   Endon↑, 2,   Fas↓, 1,   Fas↑, 2,   FasL↑, 1,   Ferroptosis↑, 1,   IAP1↓, 1,   iNOS↓, 4,   JNK↓, 1,   p‑JNK↓, 1,   MAPK↓, 4,   MAPK↑, 4,   MAPK↝, 1,   Mcl-1↓, 3,   MDM2↓, 1,   p27↑, 1,   p38↓, 3,   p38↑, 3,   PDCD4↑, 1,   PUMA⇅, 1,   survivin↓, 7,   TNFR 1↑, 2,   TRAIL↑, 3,   TRAILR↑, 2,   TumCD↑, 4,  

Kinase & Signal Transduction ⓘ

AMPKα↓, 1,   AMPKα↑, 2,   CDC7↓, 1,   HER2/EBBR2↓, 2,   RET↓, 1,   Sp1/3/4↓, 2,   TSC2↑, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 2,   cJun↑, 1,   EZH2↓, 2,   H3↓, 1,   ac‑H3↑, 2,   ac‑H4↑, 2,   miR-21↓, 3,   miR-21↑, 1,   miR-27a-3p↓, 1,   other↓, 4,   other↑, 2,   pRB↓, 1,   p‑pRB↓, 1,   Shc↓, 1,   SPP1↓, 1,   tumCV↓, 15,  

Protein Folding & ER Stress ⓘ

c-ATF6↑, 1,   ATFs↑, 1,   CHOP↓, 1,   CHOP↑, 7,   p‑eIF2α↓, 1,   ER Stress↑, 6,   GRP78/BiP↑, 7,   Hsc70↓, 1,   HSP27↓, 3,   HSP70/HSPA5↓, 3,   HSP72↓, 1,   HSP72↑, 1,   HSP90↓, 3,   HSPs↓, 2,   IRE1↑, 1,   p‑IRE1↓, 1,   NQO2↑, 1,   p‑PERK↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   BNIP3↑, 1,   LC3B-II↑, 2,   SESN2↑, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

ATM↓, 1,   BRCA1↑, 1,   CUL4B↑, 1,   DFF45↑, 2,   DNA-PK↓, 1,   DNAdam↑, 6,   DNAdamC↑, 1,   DNMT1↓, 2,   DNMT3A↓, 2,   DNMTs↓, 6,   G9a↓, 1,   MGMT↓, 1,   NKX3.1↓, 2,   NKX3.1↑, 1,   P53↓, 1,   P53↑, 15,   PARP↓, 1,   PARP↑, 3,   cl‑PARP↑, 8,   PARP1↓, 1,   PARP1↑, 1,   PCNA↓, 4,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

CDK1↓, 8,   CDK2↓, 4,   CDK2↑, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 8,   CycB/CCNB1↑, 2,   cycD1/CCND1↓, 20,   cycE/CCNE↓, 5,   cycF↓, 1,   E2Fs↓, 3,   P21↓, 2,   P21↑, 6,   RB1↑, 1,   p‑RB1↓, 1,   TAp63α↑, 1,   TumCCA↓, 1,   TumCCA↑, 31,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 2,   AR-FL↓, 1,   AR-V7↑, 1,   CD133↓, 4,   CD24↓, 2,   CD44↓, 4,   cDC2↓, 2,   cFos↓, 1,   cMET↓, 1,   CSCs↓, 14,   Diff↓, 1,   EMT↓, 15,   EP300↑, 1,   EpCAM↓, 2,   ERK↓, 5,   ERK↑, 3,   ERK↝, 1,   p‑ERK↓, 5,   FBXW7↝, 1,   FGF↓, 2,   FGFR2↓, 1,   FLT3↓, 1,   FOXO3↑, 1,   Gli1↓, 1,   GSK‐3β↓, 3,   H3K27ac↓, 1,   HDAC↓, 4,   HDAC1↓, 1,   HDAC11↓, 1,   HDAC2↓, 1,   HDAC4↓, 2,   HDAC6↓, 1,   HH↓, 2,   HMTs↓, 2,   IGF-1↓, 2,   IGF-1R↓, 5,   IGF-2↓, 2,   IGFBP3↑, 4,   Jun↓, 1,   Let-7↑, 1,   mTOR↓, 13,   p‑mTOR↓, 1,   Nanog↓, 2,   NF2↑, 1,   NOTCH↓, 2,   NOTCH1↓, 3,   NRAS↓, 1,   OCT4↓, 1,   P70S6K↓, 2,   PI3K↓, 12,   p‑PI3K↓, 1,   PTEN↑, 5,   RAS↓, 5,   SCF↓, 1,   Shh↓, 2,   STAT↓, 2,   STAT3↓, 9,   STAT3↑, 1,   p‑STAT3↓, 2,   STAT4↓, 1,   TCF↓, 1,   TOP2↓, 2,   TumCG↓, 15,   Wnt↓, 1,   Wnt/(β-catenin)↓, 3,  

Migration ⓘ

5LO↓, 1,   ACTA2↓, 1,   AntiAg↓, 1,   Ca+2↑, 5,   Ca+2↝, 1,   CDK4/6↓, 1,   CLDN2↓, 1,   COL1↓, 1,   COL3A1↓, 1,   CXCL12↓, 2,   E-cadherin↓, 1,   E-cadherin↑, 6,   EphB4↓, 1,   FAK↓, 2,   GnT-V↝, 1,   heparanase↝, 1,   hnRNPA1↓, 2,   Ki-67↓, 5,   KRAS↓, 1,   LEF1↓, 3,   MALAT1↓, 1,   MET↓, 1,   miR-133a-3p↑, 1,   miR-148a↓, 1,   miR-19b↓, 1,   miR-206↑, 1,   MMP-10↓, 1,   MMP2↓, 13,   MMP3↓, 1,   MMP7↓, 3,   MMP9↓, 8,   MMP9:TIMP1↓, 1,   MMPs↓, 9,   MSH2↑, 1,   MUC1↓, 1,   N-cadherin↓, 5,   NM23↑, 1,   p‑p44↓, 1,   p‑p44↑, 1,   PDGF↓, 3,   PKA↓, 1,   PKCδ↓, 2,   Rac1↓, 1,   RAGE↓, 2,   ROCK1↑, 1,   Slug↓, 6,   Snail↓, 7,   TET1↑, 2,   TGF-β↓, 5,   TIMP1↑, 1,   TIMP2↑, 2,   TIMP3↑, 1,   TSC1↑, 1,   TSP-1↑, 4,   TumCI↓, 13,   TumCMig↓, 13,   TumCP↓, 22,   TumCP↑, 1,   TumMeta↓, 8,   Twist↓, 5,   uPA↓, 4,   uPAR↓, 2,   Vim↓, 8,   α-SMA↓, 1,   α-SMA↑, 1,   β-catenin/ZEB1↓, 10,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   EGFR↓, 10,   FLT4↓, 1,   HIF-1↓, 1,   HIF-1↑, 1,   Hif1a↓, 6,   NO↓, 2,   VEGF↓, 9,   VEGFR2↓, 4,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 4,   NHE1↓, 1,   P-gp↓, 5,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 11,   CRP↓, 3,   CXCR4↓, 4,   IFN-γ↓, 2,   IKKα↓, 2,   IL10↓, 4,   IL1β↓, 2,   IL6↓, 7,   IL8↓, 2,   Inflam↓, 3,   IκB↓, 1,   JAK↓, 2,   JAK2↓, 2,   JAK3↓, 1,   Macrophages↓, 1,   Neut↓, 1,   NF-kB↓, 10,   p65↓, 1,   PSA↓, 4,   SOCS1↑, 1,   T-Cell↑, 2,   TLR4↓, 1,   TNF-α↓, 7,  

Cellular Microenvironment ⓘ

PLC↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 9,   AR↑, 1,   CDK6↓, 2,   COMT↓, 4,   CYP19↓, 1,   ER(estro)↑, 1,   FKBP5↓, 1,  

Drug Metabolism & Resistance ⓘ

ABCG2↓, 1,   BioAv↓, 3,   BioAv↑, 3,   BioAv↝, 1,   BioEnh↑, 7,   ChemoSen↑, 12,   ChemoSen↝, 1,   eff↓, 3,   eff↑, 23,   MDR1↓, 1,   MRP1↓, 1,   P450↓, 1,   RadioS↑, 2,   selectivity↑, 8,  

Clinical Biomarkers ⓘ

AR↓, 9,   AR↑, 1,   BRCA1↑, 1,   CRP↓, 3,   EGFR↓, 10,   EZH2↓, 2,   HEC1↓, 1,   HemoG↓, 1,   HER2/EBBR2↓, 2,   IL6↓, 7,   Ki-67↓, 5,   KRAS↓, 1,   LDH↑, 2,   NOS2↓, 1,   PSA↓, 4,   RAGE↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 5,   AntiTum↑, 4,   cardioP↑, 1,   chemoP↑, 4,   chemoPv↑, 6,   hepatoP↑, 1,   IMPDH1↓, 1,   IMPDH2↓, 1,   OS?, 1,   OS↑, 2,   PRAS40↓, 1,   Risk↓, 1,   TGFβR1↑, 1,   toxicity↓, 2,   TumVol↓, 7,   UBE2C↓, 1,  
Total Targets: 451

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

4-HNE↓, 1,   antiOx↓, 2,   antiOx↑, 20,   Catalase↑, 8,   Copper↓, 1,   Fenton↓, 1,   GPx↑, 6,   GSH↑, 8,   GSH⇅, 1,   H2O2↓, 1,   HO-1↑, 7,   Iron↓, 1,   Keap1↓, 3,   lipid-P↓, 11,   MDA↓, 10,   MDA↑, 1,   MPO↓, 1,   NOX4↓, 1,   NQO1↑, 1,   Nrf1↑, 1,   NRF2↓, 1,   NRF2↑, 16,   ROS↓, 31,   ROS↑, 1,   ROS⇅, 1,   SOD↑, 10,   SOD2↑, 1,   TAC↑, 1,   TAC∅, 1,   Trx↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↓, 1,   IronCh↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   MMP↑, 4,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   ALDOA↑, 1,   AMP↓, 1,   AMPK↑, 3,   CREB↑, 1,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   GPI↑, 1,   HK2↓, 1,   HK2↑, 1,   lactateProd↓, 1,   LDH↓, 2,   LDHA↑, 1,   LDL↓, 1,   NADPH↓, 2,   PFKL↑, 1,   PFKP↓, 1,   PKM1↑, 1,   PKM2↓, 3,   PONs↑, 1,   PPARα↑, 1,   SIRT1↓, 1,   SIRT1↑, 6,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 4,   p‑Akt↑, 1,   Apoptosis↓, 5,   BAX↓, 1,   Bax:Bcl2↓, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp12↓, 1,   Casp3↓, 1,   GRP58↓, 1,   iNOS↓, 5,   p‑JNK↓, 1,   MAPK↓, 3,   MAPK↑, 1,   p38↓, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 1,  

Protein Folding & ER Stress ⓘ

ATF6↓, 2,   CHOP↓, 2,   ER Stress↓, 6,   GRP78/BiP↓, 5,   IRE1↓, 2,   PERK↓, 1,   p‑PERK↓, 1,   UPR↓, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes ⓘ

MitoP↑, 1,  

DNA Damage & Repair ⓘ

P53↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   PI3K↓, 1,   PI3K↑, 4,   STAT3?, 1,   p‑STAT3↓, 1,  

Migration ⓘ

5LO↓, 1,   AntiAg↑, 2,   AP-1↓, 2,   Ca+2↓, 2,   CDK5↓, 1,   PKCδ↓, 1,   p‑SMAD2↓, 1,   SPARC↓, 1,   TXNIP↓, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   angioG↑, 1,   CLDN5↑, 1,   EGFR↓, 1,   Hif1a↑, 2,   NO↓, 1,   PDI↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,   BBB↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 8,   CRP↓, 1,   CXCL1↓, 1,   HMGB1↓, 2,   ICAM-1↓, 1,   IFN-γ↑, 1,   IKKα↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 7,   IL6↓, 8,   IL8↓, 2,   Inflam↓, 26,   JAK2↑, 1,   MCP1↓, 1,   NF-kB↓, 12,   p65↓, 1,   TLR4↑, 1,   TNF-α↓, 10,  

Synaptic & Neurotransmission ⓘ

AChE↓, 6,   BChE↓, 1,   BDNF↑, 2,   tau↓, 1,   p‑tau↓, 2,   TrkB↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 6,   BACE↓, 2,   NLRP3↓, 4,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 10,   BioAv↝, 1,   BioEnh↑, 3,   Dose↑, 1,   eff↓, 1,   eff↑, 4,   eff↝, 2,   Half-Life↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BG↓, 1,   BP↓, 3,   CRP↓, 1,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 8,   LDH↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 10,   cognitive↑, 8,   hepatoP↑, 3,   memory↑, 4,   motorD↑, 2,   neuroP↑, 17,   Pain↓, 2,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,   Weight↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Sepsis↓, 3,  
Total Targets: 175

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:140  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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