ROS Cancer Research Results

ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination

Item ROS NRF2 Condition Mechanism Class Remarks
ROS">Piperlongumine +++ [D][T] ROS-dominant
ROS">Shikonin +++↓/±[D][T]ROS-dominant
ROS">Vitamin K3 (menadione) +++[D]ROS-dominant
ROS">Copper (ionic / nano) +++[Fe][F]ROS-dominant
ROS">Sodium Selenite +++[D]ROS-dominant
ROS">Juglone +++[D]ROS-dominant
ROS">Auranofin +++[D]ROS-dominant
ROS">Photodynamic Therapy (PDT) +++0[L][O₂]ROS-dominant
ROS">Radiotherapy / Radiation +++0[O₂]ROS-dominant
ROS">Doxorubicin +++[D]ROS-dominant
ROS">Cisplatin ++[D][T]ROS-dominant
ROS">Salinomycin ++[D][T]ROS-dominant
ROS">Artemisinin / DHA ++[Fe][T]ROS-dominant
ROS">Sulfasalazine ++[C][T]ROS-dominant
ROS">FMD / fasting ++[M][C][O₂]ROS-dominant
ROS">Vitamin C (pharmacologic) ++[Fe][D]ROS-dominant
ROS">Silver nanoparticles ++±[F][D]ROS-dominant
ROS">Gambogic acid ++[D][T]ROS-dominant
ROS">Parthenolide ++[D][T]ROS-dominant
ROS">Plumbagin ++[D]ROS-dominant
ROS">Allicin ++[D]ROS-dominant
ROS">Ashwagandha (Withaferin A) ++[D][T]ROS-dominant
ROS">Berberine ++[D][M]ROS-dominant
ROS">PEITC ++[D][C]ROS-dominant
ROS">Methionine restriction +[M][C][T]ROS-secondary
ROS">DCA +±[M][T]ROS-secondary
ROS">Capsaicin +±[D][T]ROS-secondary
ROS">Galloflavin +0[D]ROS-secondary
ROS">Piperine +±[D][F]ROS-secondary
ROS">Propyl gallate +[D]ROS-secondary
ROS">Scoulerine +?[D][T]ROS-secondary
ROS">Thymoquinone ±±[D][T]Dual redox
ROS">Emodin ±±[D][T]Dual redox
ROS">Alpha-lipoic acid (ALA) ±[D][M]NRF2-dominant
ROS">Curcumin ±↑/↓[D][F]NRF2-dominant
ROS">EGCG ±↑/↓[D][O₂]NRF2-dominant
ROS">Quercetin ±↑/↓[D][Fe]NRF2-dominant
ROS">Resveratrol ±[D][M]NRF2-dominant
ROS">Sulforaphane ±↑↑[D]NRF2-dominant
ROS">Lycopene 0Antioxidant
ROS">Rosmarinic acid 0Antioxidant
ROS">Citrate 00Neutral


Scientific Papers found: Click to Expand⟱
1922- JG,    Juglone induces apoptosis of tumor stem-like cells through ROS-p38 pathway in glioblastoma
- in-vitro, GBM, U87MG
tumCV↓, TumCP↓, ROS↑, p‑p38↑, eff↓, Apoptosis↑, OS↑,
1921- JG,    Juglone induces ferroptotic effect on hepatocellular carcinoma and pan-cancer via the FOSL1-HMOX1 axis
- in-vitro, PC, NA - vitro+vivo, PC, NA
TumCG↓, Ferroptosis↑, ROS↑, Iron↑, lipid-P↑, MDA↑, GSH↓, FOSL1↑, HO-1↑,
1919- JG,    The Anti-Glioma Effect of Juglone Derivatives through ROS Generation
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
ROS↑, Apoptosis↑, eff↓, eff↓,
1917- JG,    Inhibition of human leukemia cells growth by juglone is mediated via autophagy induction, endogenous ROS production, and inhibition of cell migration and invasion
- in-vitro, AML, HL-60
selectivity↑, LC3I↑, LC3II↑, Beclin-1/ATG6↑, ROS↑, tumCV↓, Dose↝, TumAuto↑,
4010- K+,    Potassium-sparing diuretics might reduce risk of Alzheimer's disease
- Review, AD, NA
*Risk↓, *ROS↓, *Inflam↓, *AntiAg↑,
4007- K+,    The increased potassium intake improves cognitive performance and attenuates histopathological markers in a model of Alzheimer's disease
- in-vivo, AD, NA
*p‑tau↓, *cognitive↑, *Inflam↓, *ROS↓, *IL6↓, *4-HNE↓, *other↝,
8085- KAE,    Effects and Mechanisms of Kaempferol in the Management of Cancers through Modulation of Inflammation and Signal Transduction Pathways
- Review, Var, NA
Apoptosis↑, TumCCA↑, angioG↓, PI3K↓, Akt↓, STAT3↓, AP-1↓, NRF2↓, BioAv↑, Inflam↓, NF-kB↓, TNF-α↓, VEGF↓, BAX↑, Casp↑, Bcl-2↓, P53↑, PTEN↑, hTERT/TERT↓, NRF2↓, ROS↑, DR5↑, ERK↑, CHOP/DDIT3↑, DR4↑, JNK↑, Ki-67↓, ChemoSen↑,
8086- KAE,    Hepatoprotective Effect of Kaempferol: A Review of the Dietary Sources, Bioavailability, Mechanisms of Action, and Safety
- Review, Nor, NA
*hepatoP↑, *BioAv↝, *CYP2E1↓, *antiOx↑, *AST↓, *ALAT↓, *ROS↓, *lipid-P↓, *SIRT1↑, *GSH↑, *SOD↑, *p‑SMAD2↓, *p‑SMAD3↓, *COL1↓, *other↝,
8087- KAE,    Therapeutic Importance of Kaempferol in the Treatment of Cancer through the Modulation of Cell Signalling Pathways
- Review, Var, NA
TumCCA↓, ROS↝, Apoptosis↑, TumCP↑, TumMeta↓, angioG↓, PI3K↓, EMT↓, Snail↓, E-cadherin↓, N-cadherin↓, MMP2↓, Casp9↑, Casp7↑, PARP↑, Apoptosis↑, *ROS↓, Hif1a↓, p‑Akt↓, P53↑, cMyc↓, Glycolysis↓, PKM2↓, miR-339-5p↝, BioAv↓,
8090- KAE,    A systematic review of anti-cancer roles and mechanisms of kaempferol as a natural compound
- Review, Nor, NA
*cardioP↑, *AntiCan↑, *Inflam↓, *neuroP↑, *BioAv↓, selectivity?, p‑Akt↓, p‑cycD1/CCND1↓, p‑CDK4↓, p‑BID↓, p‑Mcl-1↓, p‑BRCA1↑, ATM↑, P53↑, P21↑, p38↑, BAX↑, BID↑, MMP↓, Casp3↑, Casp7↑, Casp9↑, AIF↑, ER Stress↑, TumMeta↓, ERK↓, AP-1↓, JNK↓, p38↓, GLUT1↓, GlucoseCon↓, MMP9↓, CYP1A1↓, ChemoSen↑, OCT4↓, Nanog↓, P-gp/ABCB1↓, ALDH1A1↓, TumCCA↑, DNAdam↑, γH2AX↑, COX2/PTGS2↓, i-ROS↓, Ca+2↓, eff↑, DR5↑, ChemoSen↑, Akt↓, PI3K↓, ROS↑, EMT↓, survivin↓,
8093- KAE,    Kaempferol inhibits Nrf2 signalling pathway via downregulation of Nrf2 mRNA and induces apoptosis in NSCLC cells
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H460
GSTA1↓, NQO1↓, HO-1↓, NRF2↓, ROS↑, Apoptosis↑,
8095- KAE,    Kaempferol: A Key Emphasis to Its Anticancer Potential
- Review, Var, NA
*AntiBio↑, *Inflam↓, *AntiTum↓, *antiOx↑, *cardioP↑, *neuroP↑, *AntiDiabetic↑, Risk↓, TumCCA↑, EMT↓, PI3K↓, Akt↓, MMP2↓, Casp3↑, Casp7↑, Casp9↑, PARP↑, *ROS↓, angioG↓, *BioAv↑, BioAv↑, selectivity↑, GLUT1↓, MCT1↓, ROS↓, ROS↑, Trx↓, Cyt‑c↑, MMP↓, miR-21↓, SOCS-3↓, STAT3↓, CDK1↓, CycB/CCNB1↑, HIF-1↓, JAK1↑, PTEN↑,
8097- KAE,    The Phenolic compound Kaempferol overcomes 5-fluorouracil resistance in human resistant LS174 colon cancer cells
- in-vitro, CRC, LS174T
ChemoSen↑, tumCV↓, Apoptosis↑, TumCCA↑, ROS↓, Casp3↑, Casp9↑, cl‑PARP↑, p‑STAT3↓, Akt↓, FOXO3↓, NF-kB↓, VEGF↓, TS↓, TK1↓,
8104- KAE,    A comprehensive and mechanistic review on protective effects of kaempferol against natural and chemical toxins: Role of NF-κB inhibition and Nrf2 activation
- Review, Nor, NA
*ROS↓, *Inflam↓, *TNF-α↓, *IL6↓, *COX2/PTGS2↓, *NF-kB↓, *hepatoP↑, *RenoP↑, *cardioP↑, *neuroP↑,
8105- KAE,    Chemo-preventive and therapeutic effect of the dietary flavonoid kaempferol: A comprehensive review
- Review, Var, NA
Apoptosis↑, tumCV↓, TumCCA↑, PI3K↓, Akt↓, EMT↓, N-cadherin↓, E-cadherin↓, Slug?, Snail?, MMP2↓, MMP9↓, CTSB↓, CTSD↓, Casp3↑, Casp8↑, Casp9↑, TIMP2↓, Akt↓, TumCD↑, i-Ca+2↑, MMP↓, *ROS↓, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *AST↓, *ALAT↓, *MDA↓, *CYP2E1↓, *NRF2↑, *AGEs↓, *IL6↓, *TNF-α↓, *NF-kB↓, *Casp3↓, *BAX↓, *antiAll↑, *COX2/PTGS2↓, *PGE2↓, *RUNX2↑, *BMP2↑, *COL1↑, *p62↑, *FASN↓, *DGAT1↓, FOXP3↑, DNAdam↑, ROS↑, Catalase↓, *ROS↓, *MMP↑, *Cyt‑c↓,
8071- KAE,    Cellular reprogramming and signaling control by kaempferol in colorectal cancer
- Review, CRC, NA
*toxicity↓, Risk↓, MMPs↓, VEGF↓, VEGFR1↓, Wnt↓, β-catenin/ZEB1↑, PI3K↓, Akt↓, mTOR↓, ChemoSen↑, *BioAv↓, TumCCA↑, Apoptosis↑, Hif1a↓, ROS↑, TumCMig↓, TumMeta↓, PKM2↓, Glycolysis↓, DNAdam↑, HO-1↑, Ferroptosis↑, eff↑, Dose↝, BioAv↑,
8070- KAE,    Kaempferol: Paving the path for advanced treatments in aging-related diseases
- Review, AD, NA
*ROS↓, *Inflam↓, *neuroP↑, *NF-kB↓, *Akt↝, *β-catenin/ZEB1↝, *Aβ↓, *BDNF↑, Apoptosis↑, TumCCA↑, EMT↓, PI3K↓,
8072- KAE,    Natural defense against colorectal cancer: the effects of kaempferol on epigenetics, apoptosis, inflammation, oxidative stress, and cell proliferation
- Review, CRC, NA
AntiCan↑, TumCP↓, TumCI↓, Inflam↓, angioG↓, ROS↑, Apoptosis↑, ChemoSen↑, Risk↓, *antiOx↑, *Inflam↓, *AntiBio↑, *cardioP↑, *neuroP↑, selectivity↑, PUMA↑, Cyt‑c↑, cl‑Casp3↑, cl‑PARP↑, Apoptosis↑, NF-kB↓, COX2/PTGS2↓, CC(CDKs/cyclins)↓, TumCCA↑, BioAv↓, eff↑, DR4↑, DR5↑, Casp3↑, Casp9↑, Casp7↑, TumCP↓, TumCI↓, TumAuto↑, mtDam↑, P53↑, MAPK↑, *lipid-P↓, *TAC↑, *Catalase↑, *SOD↑, *GPx↑, *NRF2↑,
8073- KAE,    Kaempferol inhibits oxidative stress-induced ferroptosis via the ROS/P38MAPK pathway to delay intervertebral disc degeneration: a combinatorial study of cell, animal, and transcriptomic evidence
- Review, Nor, NA
*Inflam↓, *antiOx↑, *ROS↓, *MAPK↓, *Ferroptosis↓,
8077- KAE,    Kaempferol exerts anti-colorectal cancer effects through its multi-target mediated glucose metabolism remodeling
- in-vitro, CRC, NA
AntiTum↑, Glycolysis↓, PPP↓, OXPHOS↑, ROS↑, MMP↓, Apoptosis↑, TKT↓, ALDOA↓, TumCP↓,
8080- KAE,    Hepatoprotective Effect of Kaempferol—A Review
- Review, Nor, NA
*hepatoP↑, *SIRT1↑, *AMPK↑, *TLR4↓, *NF-kB↓, *GutMicro↑, *Dose↝, *BioAv↓, *BioAv↑, *CYP2E1↓, *lipidLev↓, *COX2/PTGS2↓, *IL1β↓, *TNF-α↓, *IL6↓, *NO↓, *PGE2↓, *iNOS↓, *SOD↑, *MDA↓, *ROS↓, *AST↓, *ALAT↓, *GSH↑, *SOD↑, *Cyt‑c↓, *BAX↓, *Casp3↓, *Casp8↓, *Casp9↓, *COL1↓, *p‑SMAD2↓, *p‑SMAD3↑, *α-SMA↓, *TGF-β↓, *P450↝, *P-gp/ABCB1↓, *BioEnh↑,
8081- KAE,    The Anticancer Effects and Therapeutic Potential of Kaempferol in Triple-Negative Breast Cancer
- Review, BC, NA
*antiOx↓, *Inflam↓, *neuroP↓, *AntiCan↑, DNAdam↓, Casp3↑, Casp9↑, p‑AMT/GCST/T-protein↑, ROS↑, NRF2↑, Apoptosis↑, cl‑PARP↓, BAX↑, Bcl-2↓, TumCCA↓, angioG↓, MMP3↓, MMP9↓, ChemoSen↑, BioAv↓, Glycolysis↓, cl‑PARP↑, Ca+2↑, MMP↓, ER Stress↑, GRP78/BiP↑, CHOP/DDIT3↑, ATF6↑, angioG↓, VEGF↓, Hif1a↓, chemoP↑, *ROS↓, NRF2↑, BioAv↑,
8083- KAE,    Kaempferol stimulation of autophagy regulates the ferroptosis under the oxidative stress as mediated with AMP-activated protein kinase
- vitro+vivo, Nor, HepG2
*hepatoP↑, *ROS↓,
7827- KAE,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, *Learn↑, *memory↑, *antiOx↑, *Inflam↓, *Aβ↓, *cognitive↑, *BDNF↑, *TrkB↑, *CREB↑, *ERβ/ESR2↑, *ERK↑, *ROS↓, *AChE↓, *Dose↑,
8054- KAE,    Kaempferol Improves Alzheimer's Disease by Inhibiting Neuronal Ferroptosis via Activating GPX4/AKR1C3 Signaling Pathway
- vitro+vivo, AD, NA
*AKR1B10↝, *MDA↓, *ROS↓, *GSH↑, *SOD↑, *GPx4↑, *NQO1↑, *xCT/SLC7A11↑, *NRF2↑, *HO-1↑, *cognitive↑, *Aβ↓, *p‑tau↓, *Ferroptosis↓, *AKR1C3/17β-HSD5/PGF Synthase↑, *AKR1B1/ALR2↑,
8055- KAE,    Molecular Mechanisms of the Anticancer Activity of the Flavonoid Kaempferol: A Comprehensive Review
- Review, Var, NA
antiNeop↑, *toxicity↓, TumCCA↑, ROS↑, ER Stress↑, TumAuto↑, Pyro↑, Ferroptosis↑, angioG↓, Imm↝, eff↑, ChemoSen↑, MPT↑, MMP↓, mtDam↑, Cyt‑c↑, Bax:Bcl2↑, Fas↑, DR4↑, DR5↑, JNK↑, ERK↑, CHOP/DDIT3↑, ER Stress↑, UPR↑, Ca+2↑, PI3K↓, Akt↓, mTOR↓, AMPK↑, *Ferroptosis↓, *antiOx↑, *NRF2↑, *GPx4↑, *ROS↓, *MDA↓, *i-Iron↓, *xCT/SLC7A11↑, VEGF↓, Wnt↓, β-catenin/ZEB1↓, EMT↓, STAT3↓, M2 MC↓, MCP1/CCL2↓, MMP9↓, MMP2↓, TIMP2↓, ChemoSen↑, PKM2↑, Glycolysis↓, CSCs↓, SOX4↓, OCT4↓, CD44↓, Nanog↓, MDR1↓, *GutMicro↑,
8056- KAE,    Kaempferol: advances in biosynthesis, molecular mechanisms, and therapeutic applications
- Review, Var, NA - Review, Diabetic, NA
*antiOx↑, *ROS↓, *NRF2↑, *Inflam↓, *NF-kB↓, *MAPK↓, *STAT↓, *AntiDiabetic↑, *AMPK↑, *IRes↑, Apoptosis↑, TumCCA↑, TumMeta↓, PI3K↓, Akt↓, Wnt↓, β-catenin/ZEB1↓, *AntiBio↑, *hepatoP↑, *SIRT1↝, *BioAv↓,
8112- LA,    Metabolomics and proteomics reveal the inhibitory effect of Lactobacillus crispatus on cervical cancer
- in-vitro, Cerv, SiHa
HO-1↝, ACSL4↝, Ferroptosis↑, T-cadherin↑, ROS↑, lipid-P↑,
2351- lamb,    Anti-Warburg effect via generation of ROS and inhibition of PKM2/β-catenin mediates apoptosis of lambertianic acid in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
proCasp3↓, proPARP↓, LDHA↓, Glycolysis↓, HK2↓, PKM2↓, lactateProd↓, p‑STAT3↓, cycD1/CCND1↓, cMyc↓, β-catenin/ZEB1↓, p‑GSK‐3β↓, ROS↑, eff↓, Warburg↓,
8150- lamb,    Reactive oxygen species dependent phosphorylation of the liver kinase B1/AMP activated protein kinase/ acetyl-CoA carboxylase signaling is critically involved in apoptotic effect of lambertianic acid in hepatocellular carcinoma cells
- in-vitro, HCC, HepG2 - in-vitro, HCC, SK-HEP-1
lipidLev↓, TumCCA↑, cl‑Casp3↑, cl‑PARP↑, AMPK↑, Akt↓, mTOR↓, Bcl-2↓, Bcl-xL↓, COX2/PTGS2↓, ROS↑, eff↓, p‑STK11/LKB1↑, p‑ACC↑, *Obesity↓, *Stress↓, *antiAll↑, tumCV↓, selectivity↑, TumCP↓,
8156- lamb,    A review on chemistry, source and therapeutic potential of lambertianic acid
- Review, Var, NA
*Obesity↓, *AntiCan↑, *AMPK↑, *β-HEX↓, NA↑, TumCCA↑, AMPK↑, ACC↑, p‑Akt↓, FOXM1↓, CycB/CCNB1↓, XIAP↓, Bcl-2↓, p‑STAT3↓, p‑NF-kB↓, Bcl-xL↓, survivin↓, VEGF↓, COX2/PTGS2↓, cMyc↓, IL6↓, TNF-α↓, ROS↑, STK11/LKB1↑, cl‑Casp3↑, cl‑PARP↑, eff↑, AR↓, TumCP↓, p‑P53↓, P21↓, p27/CDKN1B↓, cycD1/CCND1↓, CDK4↓, PSA↓, STAT3↓, ac‑p65↓, *antiAll↑,
8157- lamb,    Pinus koraiensis leaf extract and lambertianic acid attenuate fatigue and improve endurance capacity via PI3K-mediated regulation of oxidative stress and mitochondrial biogenesis
- in-vivo, Nor, NA
*fatigue↓, *ROS↓, *NF-kB↓, *IL6↓, *SOD↑, *PI3K↑, *NRF2↑, *HO-1↑, *SIRT1↑, *PGC-1α↑, *Nrf1↑, *Strength↑,
8169- Lap,    Lapatinib Activates the Kelch-Like ECH-Associated Protein 1-Nuclear Factor Erythroid 2-Related Factor 2 Pathway in HepG2 Cells
- in-vitro, Liver, HepG2
toxicity↑, mtDam↑, ROS↑, NRF2↑, GSH↑, GSSG↑, SOD2↑,
8167- LapC,    Characterization of lapachol cytotoxicity: contribution of glutathione depletion for oxidative stress in Saccharomyces cerevisiae
- in-vitro, Nor, NA
*GSH↓, *SOD1↓, *lipid-P↑, *ROS↑,
8232- LCA,    Licochalcone A induces G2/M phase arrest and apoptosis via regulating p53 pathways in esophageal cancer: In-vitro and in-vivo study
- vitro+vivo, ESCC, NA
TumCP↓, TumCMig↓, TumCI↓, MMPs↓, ROS↑, MMP↓, BAX↑, Casp3↑, Casp9↑, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, CycB/CCNB1↓, CDK1↓, P53↑, TumCG↓, toxicity↓,
8235- LCA,    Anticancer effects of licochalcones: A review of the mechanisms
- Review, Var, NA
mt-Apoptosis↑, TumAuto↑, TumCMig↓, LC3‑Ⅱ/LC3‑Ⅰ↑, ATG5↑, ATG7↑, p62↑, CHOP/DDIT3↑, ER Stress↑, UPR↑, ATG3↑, Beclin-1/ATG6↑, ATG16L1↑, PERK↑, ATF4↑, ATP↓, Hif1a↓, GLUT1↓, PDK1 / PDPK1↓, Bcl-xL↓, Bcl-2↓, BAD↑, BAX↑, Casp3↑, survivin↓, EGFR↓, ERK↓, Akt↓, mtDam↑, MMP↓, Cyt‑c↑, Casp↑, MDM2↓, CycB/CCNB1↓, CDC2↓, CDC25↓, TumCCA↑, TumCP↓, Wnt↓, β-catenin/ZEB1↓, Sp1/3/4↓, MMP-10↓, MMP3↓, TumCI↓, Imm↑, PD-L1↓, ROS↑, 4E-BP1↓, eIF2α↓, PI3K↓, mTOR↓, p‑cMET↑, Ca+2↑, RUBCN↓, ATG13↑, TSC1↑, TSC2↑, PRAS40↑, PP2A↑, ULK1/ATG1↑, THEM4/CTMP↑, DR5↑, Fas↑, TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, PKCδ↓, P70S6K↓, VEGF↓, angioG↓, HK2↓, Glycolysis↓, TrxR1↓, APAF1↑, cl‑PARP↑, Bax:Bcl2↑, ABCG2↓, BioEnh↑,
8261- LCA,    Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels
- in-vitro, CRC, T24/HTB-9
TumCP↓, ROS↑, Apoptosis↑, ER Stress↑, i-Ca+2↑, MMP↓, APAF1↑, Casp9↑, Casp3↑, cal2↑, CASP4↑,
8237- LCA,    Role of Licochalcone A in Potential Pharmacological Therapy: A Review
- Review, Var, NA
*other↝, *Inflam↓, *Bacteria↓, *antiOx↑, *AntiP↑, *neuroP↑, *glucose↝, *lipid-P↓, PKCδ↓, P70S6K↓, Akt↓, ER Stress↑, Apoptosis↑, Ca+2↑, PI3K↓, mTOR↓, Casp3↑, Bcl-2↓, Cyt‑c↑, BAX↑, cl‑PARP↑, cycD1/CCND1↑, ROS↑, CHOP/DDIT3↑, ERK↑, p38↑, JNK↓, IAP1↓, XIAP↓, survivin↓, cFLIP↓, RIP1↓, EGFR↓, MET↓, HER2/EBBR2↓, p‑4E-BP1↓, PERK↑, eIF2α↑, PD-L1↓, HK2↓, Glycolysis↓, Sp1/3/4↓, FasL↑, MMP↓, ATP↓, TumAuto↑, WEE1↑, P21↑, CDK1↓, TumCCA↑, TumCMig↓, TumCI↓, ABCG2↓, HSP90↓, T-Cell↑, CD4+↑, CD25+↑, FOXP3↑, Imm↝, *Inflam↓, *NF-kB↓, *NRF2↑, *AntiArt↑,
8260- LCA,    Licochalcone A Induces Ferroptosis in Hepatocellular Carcinoma via Reactive Oxygen Species Activated by the SLC7A11/GPX4 Pathway
- vitro+vivo, Liver, HepG2 - in-vitro, Liver, HUH7
tumCV↑, xCT/SLC7A11↓, Ferroptosis↑, GPx4↑, ROS↑, TumCP↓, TumCD↑, Iron↑,
8242- LCA,    Nrf2 signaling and autophagy are complementary in protecting lipopolysaccharide/d-galactosamine-induced acute liver injury by licochalcone A
- in-vivo, LiverDam, NA
*ALAT↓, *AST↓, *Inflam↓, *ROS↓, *TLR4↓, *MAPK↓, *NF-kB↓, *TXNIP↓, *NLRP3↓, *NRF2↑, *p62↑, *hepatoP↑, *autophagy↑,
8243- LCA,    Licochalcone A Inhibits Cellular Motility by Suppressing E-cadherin and MAPK Signaling in Breast Cancer
- in-vitro, BC, MDA-MB-231
Inflam↓, AntiTum↑, TumAuto↑, Sp1/3/4↓, TumCMig↓, MAPK↓, Akt↓, cl‑Casp3↑, cl‑Casp9↑, Bcl-2↓, Cyt‑c↑, TumCP↓, ROS↑, Apoptosis↑, TumCMig↓, TumCI↓, MMP↓, γH2AX↑,
8244- LCA,    Licochalcone A from licorice root, an inhibitor of human hepatoma cell growth via induction of cell apoptosis and cell cycle arrest
- in-vitro, Liver, HepG2
TumCP↓, ROS↑, TumCCA↑, Apoptosis↑, survivin↓, CycB/CCNB1↓, CDK1↓, WEE1↑, P21↑, cycD1/CCND1↑, JNK↑, TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, DR5↑, Casp3↑, Casp8↑, Casp10↑, Fas↑, BAD↑, BAX↑, PUMA↑, PKCδ↓, P70S6K↓, Akt↓,
8245- LCA,    Licochalcone A Upregulates Nrf2 Antioxidant Pathway and Thereby Alleviates Acetaminophen-Induced Hepatotoxicity
- in-vivo, LiverDam, NA
*hepatoP↑, *Apoptosis↓, *mtDam↓, *ROS↓, *NRF2↑, *Keap1↓, *ARE↑, *ALAT↓, *AST↓, *MDA↓, *MPO↓, *SOD↑, *GSH/GSSG↑, *Bcl-2↑, *BAX↓, *cl‑Casp3↓, *p‑cJun↓, *AIF↓, *Cyt‑c↓,
8254- LCA,  Geld,    Licochalcone A enhances geldanamycin-induced apoptosis through reactive oxygen species-mediated caspase activation
- in-vitro, Ovarian, NA
MMP↓, Cyt‑c↑, Casp↑, cl‑PARP1↑, ROS↑, GSH↓, eff↓,
8257- LCA,    Licochalcone A inhibiting proliferation of bladder cancer T24 cells by inducing reactive oxygen species production
- in-vitro, CRC, T24/HTB-9
TumCP↓, ROS↑, eff↓, GSH/GSSG↓,
8230- LCA,    The Ameliorative Role of Lico A on Aflatoxin B1-Triggered Hepatotoxicity Partially by Activating Nrf2 Signal Pathway
- vitro+vivo, Nor, NA
*hepatoP↑, *ROS↓, *TLR4↓, *NF-kB↓, *MAPK↓, *NLRP3↓, *NRF2↑, *Inflam↓, *Pyro↓,
8206- LCA,    Licochalcone A-induced human gastric cancer BGC-823 cells apoptosis by regulating ROS-mediated MAPKs and PI3K/AKT signaling pathways
- in-vivo, GC, BGC-823
ROS?, Casp3↑, cl‑PARP↑, eff↓, ERK↑, JNK↑, MAPK↑, AntiP↑, AntiTum↑, TumCP↓, selectivity↑, GSH/GSSG↓, MDA↑, lipid-P↑, PI3K↓, Akt↓,
8207- LCA,    Licochalcone a Induces ROS-Mediated Apoptosis through TrxR1 Inactivation in Colorectal Cancer Cells
- in-vitro, CRC, HCT116
ROS↑, TumCCA↑, Apoptosis↑, eff↓, TrxR1↓, cDC2↓, Bcl-2↓, BAX↑, NRF2↓, p‑ASK1↑,
8209- LCA,    Licochalcone A Exerts Anti-Cancer Activity by Inhibiting STAT3 in SKOV3 Human Ovarian Cancer Cells
- in-vitro, Ovarian, SKOV3
tumCV↓, TumCCA↑, ROS↑, MMP↓, Apoptosis↑, cl‑Casp↑, Cyt‑c↑, STAT3↓, TumCP↓, Dose↝, p‑STAT3↓,
8210- LCA,    Licochalcone A-Induced Human Bladder Cancer T24 Cells Apoptosis Triggered by Mitochondria Dysfunction and Endoplasmic Reticulum Stress
- in-vitro, Bladder, T24/HTB-9
chemoPv↑, TumCP↓, ROS↑, Apoptosis↑, mtDam↑, Casp3↑, cl‑PARP↑, ER Stress↑, GRP78/BiP↑, CHOP/DDIT3↑, Casp12↑, mt-ROS↑, tumCV↓, GSH/GSSG↓, NA↓,

Showing Research Papers: 1651 to 1700 of 2773
Prev Page 34 of 56 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2773

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0)

p‑AMT/GCST/T-protein↑, 1,   AntiP↑, 1,   ATG13↑, 1,   ATG16L1↑, 1,   CASP4↑, 1,   miR-339-5p↝, 1,   NA↓, 1,   NA↑, 1,   RUBCN↓, 1,   THEM4/CTMP↑, 1,   TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, 2,   ULK1/ATG1↑, 1,   WEE1↑, 2,  

Redox & Oxidative Stress(tgid=1)

Catalase↓, 1,   CYP1A1↓, 1,   Ferroptosis↑, 5,   GPx4↑, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 3,   GSSG↑, 1,   GSTA1↓, 1,   HO-1↓, 1,   HO-1↑, 2,   HO-1↝, 1,   Iron↑, 2,   lipid-P↑, 3,   MDA↑, 2,   NQO1↓, 1,   NRF2↓, 4,   NRF2↑, 3,   OXPHOS↑, 1,   ROS?, 1,   ROS↓, 2,   ROS↑, 31,   ROS↝, 1,   i-ROS↓, 1,   mt-ROS↑, 1,   SOD2↑, 1,   TKT↓, 1,   Trx↓, 1,   TrxR1↓, 2,   xCT/SLC7A11↓, 1,  

Mitochondria & Bioenergetics(tgid=3)

AIF↑, 1,   ATP↓, 2,   CDC2↓, 1,   CDC25↓, 1,   MMP↓, 13,   MPT↑, 1,   mtDam↑, 5,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4)

ACC↑, 1,   p‑ACC↑, 1,   ACSL4↝, 1,   ALDOA↓, 1,   AMPK↑, 3,   ATG7↑, 1,   cMyc↓, 3,   GlucoseCon↓, 1,   Glycolysis↓, 8,   HK2↓, 3,   lactateProd↓, 1,   LDHA↓, 1,   lipidLev↓, 1,   PDK1 / PDPK1↓, 1,   PKM2↓, 3,   PKM2↑, 1,   PPP↓, 1,   STK11/LKB1↑, 1,   p‑STK11/LKB1↑, 1,   TS↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5)

Akt↓, 15,   p‑Akt↓, 3,   APAF1↑, 2,   Apoptosis↑, 23,   mt-Apoptosis↑, 1,   p‑ASK1↑, 1,   BAD↑, 2,   BAX↑, 8,   Bax:Bcl2↑, 2,   Bcl-2↓, 8,   Bcl-xL↓, 3,   BID↑, 1,   p‑BID↓, 1,   Casp↑, 3,   cl‑Casp↑, 1,   Casp10↑, 1,   Casp12↑, 1,   Casp3↑, 13,   cl‑Casp3↑, 4,   proCasp3↓, 1,   Casp7↑, 4,   Casp8↑, 2,   Casp9↑, 9,   cl‑Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 8,   DR4↑, 3,   DR5↑, 6,   Fas↑, 3,   FasL↑, 1,   Ferroptosis↑, 5,   hTERT/TERT↓, 1,   IAP1↓, 1,   JNK↓, 2,   JNK↑, 4,   MAPK↓, 1,   MAPK↑, 2,   p‑Mcl-1↓, 1,   MCT1↓, 1,   MDM2↓, 1,   p27/CDKN1B↓, 1,   p38↓, 1,   p38↑, 2,   p‑p38↑, 1,   PUMA↑, 2,   Pyro↑, 1,   RIP1↓, 1,   survivin↓, 5,   TumCD↑, 2,  

Kinase & Signal Transduction(tgid=6)

HER2/EBBR2↓, 1,   Sp1/3/4↓, 3,   TSC2↑, 1,  

Transcription & Epigenetics(tgid=7)

miR-21↓, 1,   tumCV↓, 7,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8)

ATF6↑, 1,   CHOP/DDIT3↑, 6,   eIF2α↓, 1,   eIF2α↑, 1,   ER Stress↑, 8,   GRP78/BiP↑, 2,   HSP90↓, 1,   PERK↑, 2,   UPR↑, 2,  

Autophagy & Lysosomes(tgid=9)

ATG3↑, 1,   ATG5↑, 1,   Beclin-1/ATG6↑, 2,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3I↑, 1,   LC3II↑, 1,   p62↑, 1,   TumAuto↑, 6,  

DNA Damage & Repair(tgid=10)

ATM↑, 1,   p‑BRCA1↑, 1,   DNAdam↓, 1,   DNAdam↑, 3,   P53↑, 5,   p‑P53↓, 1,   PARP↑, 2,   cl‑PARP↓, 1,   cl‑PARP↑, 9,   proPARP↓, 1,   cl‑PARP1↑, 1,   γH2AX↑, 2,  

Cell Cycle & Senescence(tgid=11)

CDK1↓, 4,   CDK4↓, 1,   p‑CDK4↓, 1,   CycB/CCNB1↓, 4,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 3,   cycD1/CCND1↑, 2,   p‑cycD1/CCND1↓, 1,   P21↓, 1,   P21↑, 3,   TumCCA↓, 2,   TumCCA↑, 18,  

Proliferation, Differentiation & Cell State(tgid=12)

4E-BP1↓, 1,   p‑4E-BP1↓, 1,   ALDH1A1↓, 1,   CD44↓, 1,   cDC2↓, 1,   p‑cMET↑, 1,   CSCs↓, 1,   CTSB↓, 1,   CTSD↓, 1,   EMT↓, 6,   ERK↓, 2,   ERK↑, 4,   FOSL1↑, 1,   FOXM1↓, 1,   FOXO3↓, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 5,   Nanog↓, 2,   OCT4↓, 2,   P70S6K↓, 3,   PI3K↓, 12,   PTEN↑, 2,   STAT3↓, 5,   p‑STAT3↓, 4,   TK1↓, 1,   TumCG↓, 2,   Wnt↓, 4,  

Migration(tgid=13)

AP-1↓, 2,   Ca+2↓, 1,   Ca+2↑, 4,   i-Ca+2↑, 2,   cal2↑, 1,   CC(CDKs/cyclins)↓, 1,   E-cadherin↓, 2,   Ki-67↓, 1,   MET↓, 1,   MMP-10↓, 1,   MMP2↓, 4,   MMP3↓, 2,   MMP9↓, 4,   MMPs↓, 2,   N-cadherin↓, 2,   PKCδ↓, 3,   Slug?, 1,   Snail?, 1,   Snail↓, 1,   SOX4↓, 1,   T-cadherin↑, 1,   TIMP2↓, 2,   TSC1↑, 1,   TumCI↓, 6,   TumCMig↓, 6,   TumCP↓, 16,   TumCP↑, 1,   TumMeta↓, 4,   VEGFR1↓, 1,   β-catenin/ZEB1↓, 4,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 8,   ATF4↑, 1,   EGFR↓, 2,   HIF-1↓, 1,   Hif1a↓, 4,   VEGF↓, 7,  

Barriers & Transport(tgid=15)

GLUT1↓, 3,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

CD25+↑, 1,   CD4+↑, 1,   COX2/PTGS2↓, 4,   FOXP3↑, 2,   IL6↓, 1,   Imm↑, 1,   Imm↝, 2,   Inflam↓, 3,   JAK1↑, 1,   M2 MC↓, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 3,   p‑NF-kB↓, 1,   ac‑p65↓, 1,   PD-L1↓, 2,   PSA↓, 1,   SOCS-3↓, 1,   T-Cell↑, 1,   TNF-α↓, 2,  

Protein Aggregation(tgid=19)

PP2A↑, 1,  

Hormonal & Nuclear Receptors(tgid=20)

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21)

ABCG2↓, 2,   BioAv↓, 3,   BioAv↑, 4,   BioEnh↑, 1,   ChemoSen↑, 9,   Dose↝, 3,   eff↓, 9,   eff↑, 5,   MDR1↓, 1,   selectivity?, 1,   selectivity↑, 5,  

Clinical Biomarkers(tgid=22)

AR↓, 1,   p‑BRCA1↑, 1,   EGFR↓, 2,   FOXM1↓, 1,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   Ki-67↓, 1,   PD-L1↓, 2,   PSA↓, 1,  

Functional Outcomes(tgid=23)

AntiCan↑, 1,   antiNeop↑, 1,   AntiTum↑, 3,   chemoP↑, 1,   chemoPv↑, 1,   OS↑, 1,   PRAS40↑, 1,   Risk↓, 3,   toxicity↓, 1,   toxicity↑, 1,  
Total Targets: 286

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

AKR1B1/ALR2↑, 1,   AKR1B10↝, 1,   AKR1C3/17β-HSD5/PGF Synthase↑, 1,   antiAll↑, 3,   AntiArt↑, 1,   AntiBio↑, 3,   AntiP↑, 1,   autophagy↑, 1,   IRes↑, 1,   Learn↑, 1,   Stress↓, 1,   β-HEX↓, 1,  

Redox & Oxidative Stress(tgid=1)

4-HNE↓, 1,   antiOx↓, 1,   antiOx↑, 8,   ARE↑, 1,   Catalase↑, 2,   CYP2E1↓, 3,   Ferroptosis↓, 3,   GPx↑, 2,   GPx4↑, 2,   GSH↓, 1,   GSH↑, 3,   GSH/GSSG↑, 1,   GSTs↑, 1,   HO-1↑, 2,   i-Iron↓, 1,   Keap1↓, 1,   lipid-P↓, 3,   lipid-P↑, 1,   MDA↓, 5,   MPO↓, 1,   NQO1↑, 1,   Nrf1↑, 1,   NRF2↑, 10,   ROS↓, 21,   ROS↑, 1,   SOD↑, 8,   SOD1↓, 1,   TAC↑, 1,   xCT/SLC7A11↑, 2,  

Mitochondria & Bioenergetics(tgid=3)

AIF↓, 1,   MMP↑, 1,   mtDam↓, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

ALAT↓, 5,   AMPK↑, 3,   CREB↑, 1,   DGAT1↓, 1,   FASN↓, 1,   glucose↝, 1,   lipidLev↓, 1,   SIRT1↑, 3,   SIRT1↝, 1,  

Cell Death(tgid=5)

Akt↝, 1,   Apoptosis↓, 1,   BAX↓, 3,   Bcl-2↑, 1,   BMP2↑, 1,   Casp3↓, 2,   cl‑Casp3↓, 1,   Casp8↓, 1,   Casp9↓, 1,   Cyt‑c↓, 3,   Ferroptosis↓, 3,   iNOS↓, 1,   MAPK↓, 4,   Pyro↓, 1,  

Transcription & Epigenetics(tgid=7)

p‑cJun↓, 1,   other↝, 3,  

Autophagy & Lysosomes(tgid=9)

p62↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12)

ERK↑, 1,   PI3K↑, 1,   RUNX2↑, 1,   STAT↓, 1,  

Migration(tgid=13)

AntiAg↑, 1,   COL1↓, 2,   COL1↑, 1,   p‑SMAD2↓, 2,   p‑SMAD3↓, 1,   p‑SMAD3↑, 1,   TGF-β↓, 1,   TXNIP↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↝, 1,  

Angiogenesis & Vasculature(tgid=14)

NO↓, 1,  

Barriers & Transport(tgid=15)

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 3,   IL1β↓, 1,   IL6↓, 5,   Inflam↓, 15,   NF-kB↓, 9,   PGE2↓, 2,   TLR4↓, 3,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18)

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

Protein Aggregation(tgid=19)

AGEs↓, 1,   Aβ↓, 3,   NLRP3↓, 2,  

Hormonal & Nuclear Receptors(tgid=20)

ERβ/ESR2↑, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 4,   BioAv↑, 2,   BioAv↝, 1,   BioEnh↑, 1,   Dose↑, 1,   Dose↝, 1,   P450↝, 1,  

Clinical Biomarkers(tgid=22)

ALAT↓, 5,   AST↓, 5,   GutMicro↑, 2,   IL6↓, 5,  

Functional Outcomes(tgid=23)

AntiCan↑, 3,   AntiDiabetic↑, 2,   AntiTum↓, 1,   cardioP↑, 4,   cognitive↑, 3,   fatigue↓, 1,   hepatoP↑, 8,   memory↑, 1,   neuroP↓, 1,   neuroP↑, 7,   Obesity↓, 2,   RenoP↑, 1,   Risk↓, 1,   Strength↑, 1,   toxicity↓, 2,  

Infection & Microbiome(tgid=24)

Bacteria↓, 1,  
Total Targets: 130

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
122 Silver-NanoParticles
99 Curcumin
95 Quercetin
91 Magnetic Fields
74 Thymoquinone
58 Resveratrol
57 Vitamin C (Ascorbic Acid)
55 Radiotherapy/Radiation
55 Shikonin
50 Berberine
50 Sulforaphane (mainly Broccoli)
47 Lycopene
47 Hydrogen Gas
45 EGCG (Epigallocatechin Gallate)
43 Baicalein
42 Alpha-Lipoic-Acid
40 Selenite (Sodium)
40 Ashwagandha(Withaferin A)
40 Piperlongumine
39 Selenium NanoParticles
38 Artemisinin
37 Betulinic acid
34 Rosmarinic acid
34 Fisetin
33 Capsaicin
32 Silymarin (Milk Thistle) silibinin
29 Cisplatin
29 Chemotherapy
29 Propolis -bee glue
28 Copper and Cu NanoParticles
28 Apigenin (mainly Parsley)
28 Honokiol
27 doxorubicin
26 Allicin (mainly Garlic)
26 Emodin
26 Gambogic Acid
25 Luteolin
25 Magnetic Field Rotating
25 Phenethyl isothiocyanate
23 Chlorogenic acid
23 Chrysin
23 Juglone
22 Kaempferol
22 Vitamin K2
21 chitosan
21 Licochalcone A
20 Coenzyme Q10
19 isoquercitrin
19 isoorientin
18 Boron
18 Ferulic acid
17 salinomycin
17 Ivermectin
17 Parthenolide
16 Urolithin
15 Caffeic acid
15 chaetocin
15 Ellagic acid
15 Eugenol
15 Isoliquiritigenin
14 Photodynamic Therapy
14 Auranofin
14 Boswellia (frankincense)
14 Carnosic acid
14 Carvacrol
14 Selenium
14 Crocetin
14 Phenylbutyrate
13 Dichloroacetate
13 Dandelion Root
13 Gallic acid
13 Pterostilbene
12 Melatonin
12 Graviola
12 HydroxyTyrosol
12 Isobavachalcone
12 VitK3,menadione
11 5-fluorouracil
11 Astaxanthin
11 Cinnamon
11 Cynaropicrin
11 Hyperthermia
11 Isovitexin
11 Piperine
10 Beta-Caryophyllene
10 α-Bisabolol / Chamomile oil
10 Ursolic acid
10 diet FMD Fasting Mimicking Diet
10 Hyperoside
10 Plumbagin
10 Nimbolide
9 SonoDynamic Therapy UltraSound
9 Andrographis
9 D-limonene
9 Bacopa monnieri
9 borneol
9 Centella asiatica / Gotu kola → asiaticoside
9 Hydroxycinnamic-acid
9 Diclofenac
9 Ginkgo biloba
8 3-bromopyruvate
8 Rutin
8 Disulfiram
8 Electrical Pulses
8 Sulfasalazine
8 Methylene blue
8 Moringa oleifera
8 Propyl gallate
7 EMF
7 Gold NanoParticles
7 Gemcitabine (Gemzar)
7 Metformin
7 immunotherapy
7 Berbamine
7 brusatol
7 Carnosine
7 Celastrol
7 diet Methionine-Restricted Diet
7 eicosapentaenoic acid
7 Formononetin
7 Garcinol
7 Ginkgetin
6 2-DeoxyGlucose
6 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
6 Anethole/trans-Anethole
6 Docetaxel
6 Biochanin A
6 Butyrate
6 Mung Bean Sprouts
6 Chlorophyllin
6 Chocolate
6 Citric Acid
6 Carvone
6 Cynara scolymus/Globe Artichoke/Artichoke Extract
6 Lemongrass Extract/Citral
6 Aflavin-3,3′-digallate
6 Fenbendazole
6 Fucoidan
6 HydroxyCitric Acid
6 Vitexin
5 1,8-Cineole
5 Brucea javanica
5 Bromelain
5 erastin
5 buckwheat sprouts
5 Thymol-Thymus vulgaris
5 Cichoric acid / Chicoric acid
5 Spermidine
5 Huperzine A/Huperzia serrata
5 Date Fruit Extract
5 Docosahexaenoic Acid
5 Evodiamine
5 Gossypol/AT-101
5 Magnolol
5 nicotinamide adenine dinucleotide
4 chemodynamic therapy
4 Zinc
4 Vitamin E
4 Cucurbitacin
4 diet Short Term Fasting
4 Ginkgo biloba-EGb 761
4 Geraniol
4 Ginkgolide B
4 Ginseng
4 γ-linolenic acid (Borage Oil)
4 Hibiscus sabdariffa
4 Inositol
4 lambertianic acid
4 Lactoferrin/Talactoferrin
4 Linalool
4 Magnesium
4 Naringin
4 Taurine
3 5-Aminolevulinic acid
3 Anthocyanins
3 Glucose
3 temozolomide
3 Black phosphorus
3 Paclitaxel/Taxol
3 Caffeic Acid Phenethyl Ester (CAPE)
3 Catechins
3 Choline
3 Dihydrocaffeic Acid
3 Oxygen, Hyperbaric
3 ferumoxytol
3 flavonoids
3 Shilajit/Fulvic Acid
3 Ginger/6-Shogaol/Gingerol
3 Grapeseed extract
3 Orlistat
3 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
3 MCToil
3 Methylsulfonylmethane
3 Mushroom Lion’s Mane
3 Myricetin
3 Oleuropein
3 α-Santalol/Sandalwood oil
3 Shankhpushpi
3 Terpinen-4-ol / Tea Tree Oil
3 Turmerones
3 Vitamin B1/Thiamine
2 5-Hydroxytryptophan
2 Astragalus
2 DTS(dibenzyl trisulphide) from Anamu
2 Fennel Oil/Foeniculum vulgare
2 Aromatherapy
2 Ascorbyl Palmitate
2 Atorvastatin
2 Aloe anthraquinones
2 beta-glucans
2 Baicalin
2 Lapatinib
2 xanthohumol
2 Cannabidiol
2 beta-carotene(VitA)
2 Bufalin/Huachansu
2 Bruteridin(bergamot juice)
2 Bullatacin
2 Cat’s Claw
2 Celecoxib
2 methotrexate
2 Carica papaya leaf extract
2 Calorie Restriction Mimetics
2 Galantamine
2 CUSP9
2 Folic Acid, Vit B9
2 Galloflavin
2 Germanium Organic/Ge-132 / propagermanium (organogermanium)
2 iodine
2 isoflavones
2 Potassium
2 Methyl Jasmonate
2 Methylglyoxal
2 Vitamin B3,Niacin
2 Niclosamide (Niclocide)
2 Pachymic acid
2 Sanguinarine
2 Psoralidin
2 Radio Frequency
2 Rauwolfia serpentina/Indian Snakeroot
2 Sesame seeds and Oil
2 Iron
2 Salvia miltiorrhiza
2 triptolide
2 Vitamin D3
1 cetuximab
1 Annona atemoya Leaf Extract
1 Annona atemoya Seed Extract
1 Anzaroot, Astragalus fasciculifolius Bioss
1 entinostat
1 Camptothecin
1 Resiquimod
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 alpha Linolenic acid
1 Angelica archangelica / Garden Angelica
1 Anti-oxidants
1 Sorafenib (brand name Nexavar)
1 tamoxifen
1 almonertinib
1 epirubicin
1 Ras-selective lethal 3
1 Black Seed Oil/Nigella sativa
1 Lecithin
1 Chyawanprash
1 Aspirin
1 methylseleninic acid
1 Rivastigmine
1 Cyclopamine
1 Cysteamine
1 Dichloroacetophenone(2,2-)
1 Deguelin
1 diet Fermented Foods
1 diet Ketogenic
1 diet Plant based
1 Echinacea
1 Cannabichromene
1 Exercise
1 olaparib/LYNPARZA
1 verapamil
1 hydroxychloroquine
1 Ginkgolic acids
1 Genistein (soy isoflavone)
1 Germanium inorganic
1 hydrogen sulfide
1 Helleborus niger extracts – Christmas Rose
1 Rapamycin
1 Indole-3-carbinol
1 Inoscavin A
1 Butein
1 Scopoletin
1 Morin
1 Lactobacillus
1 Lapachol
1 Geldanamycin
1 Licorice
1 Myrrh
1 N-Acetyl-Cysteine
1 No Product/Mechanism Only
1 Oleocanthal
1 sericin
1 Polyphenols
1 benzo(a)pyrene
1 Rhein
1 Perilla
1 Salvia officinalis
1 Oxaliplatin
1 Scoulerine
1 polyethylene glycol
1 acetaminophen
1 Silicic Acid
1 Squalene
1 Osimertinib
1 Adagrasib
1 Glutathione
1 statins
1 Safflower yellow
1 Terminalia bellirica
1 Triphala
1 Vanillic Acid
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B2,Riboflavin
1 Vitamin B5,Pantothenic Acid
1 glucose deprivation
1 Transarterial Chemoembolization
1 probiotics
1 Zinc Oxide
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#:%  Target#:275  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

Home Page