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)

"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
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
4435- AgNPs,  Gluc,    Glucose-Functionalized Silver Nanoparticles as a Potential New Therapy Agent Targeting Hormone-Resistant Prostate Cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
selectivity↑, ROS↑, mtDam↑, TumCCA↑, TumCP↓, Apoptosis↑, MMP↓,
4584- AgNPs,    Silver Nanoparticles Synthesized Using Carica papaya Leaf Extract (AgNPs-PLE) Causes Cell Cycle Arrest and Apoptosis in Human Prostate (DU145) Cancer Cells
- in-vitro, Pca, DU145
selectivity↑, ROS↑, BAX↑, cl‑Casp3↑, p‑PARP↑, TumCCA↑, cycD1/CCND1↓, p27↑, P21↑, AntiCan↑,
2646- AL,    Anti-Cancer Potential of Homemade Fresh Garlic Extract Is Related to Increased Endoplasmic Reticulum Stress
- in-vitro, Pca, DU145 - in-vitro, Melanoma, RPMI-8226
AntiCan↑, eff↓, ChemoSen↑, ER Stress↑, tumCV↓, DNAdam↑, GSH∅, HSP70/HSPA5↓, UPR↑, β-catenin/ZEB1↓, ROS↑, HO-2↑, SIRT1↑, GlucoseCon∅, lactateProd∅, chemoP↑,
3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, TumCMig↓, TumCI↓, ROS↑, Hif1a↑, JNK↑, Casp↑, TumCCA↑, Apoptosis↑, selectivity↑,
277- ALA,    α-lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B
ROS↑, Hif1a↑, JNK↑, Casp3↑, P21↑, BAX↑, Bcl-xL↓, cFos↓,
265- ALA,    Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
ROS↓, SOD↓, GSTP1/GSTπ↓, NRF2↓, p62↓, p62↑, SOD↑, p‑mTOR↑, Beclin-1↓, ROS↑, SOD1↑,
1564- Api,    Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation
- in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
MDM2↓, NF-kB↓, p65↓, P21↑, ROS↑, GSH↓, MMP↓, Cyt‑c↑, Apoptosis↑, P53↑, eff↓, Bcl-xL↓, Bcl-2↓, BAX↑, Casp↑, TumCG↓, TumVol↓, TumW↓,
1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, selectivity↑, selectivity↓, ROS↑, eff↑, tumCV↓, MMP↓, Dose∅, eff↓, DNAdam↑, Apoptosis↑, TumAuto↑, Necroptosis↑, p‑P53↑, BIM↑, BAX↑, p‑PARP↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Bcl-2↓, AIF↑, p62↑, LC3B↑, MLKL↑, p‑MLKL↓, RIP3↑, p‑RIP3↑, TumCG↑, TumW↓,
2003- Ash,    Withaferin A Induces Cell Death Selectively in Androgen-Independent Prostate Cancer Cells but Not in Normal Fibroblast Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Nor, TIG-1 - in-vitro, PC, LNCaP
TumCD↑, selectivity↑, cFos↑, ROS↑, *ROS∅, HSP70/HSPA5↑, Apoptosis↑, ER Stress↑, TumCCA↑,
2479- Ba,    Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells
- in-vitro, HCC, SW480 - in-vitro, Pca, PC3
12LOX↓, DR5↑, CHOP↑, ROS↑, *ROS∅, selectivity↑,
1390- BBR,  Rad,    Berberine Inhibited Radioresistant Effects and Enhanced Anti-Tumor Effects in the Irradiated-Human Prostate Cancer Cells
- in-vitro, Pca, PC3
RadioS↑, Apoptosis↑, ROS↑, eff↑, BAX↑, Casp3↑, P53↑, p38↑, JNK↑, Bcl-2↓, ERK↓, HO-1↓,
1404- BBR,    Berberine-induced apoptosis in human prostate cancer cells is initiated by reactive oxygen species generation
- in-vitro, Pca, PC3
Apoptosis↑, *Apoptosis∅, MMP↓, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, ROS↑, eff↓, Cyt‑c↑,
5653- BNL,    Borneol hinders the proliferation and induces apoptosis through the suppression of reactive oxygen species-mediated JAK1 and STAT-3 signaling in human prostate cancer cells
- in-vitro, Pca, PC3
ROS↑, TumCP↓, cycD1/CCND1↓, cycE1↓, Apoptosis↑, BAX↓, Casp3↑, Bcl-2↓, IL6↓, JAK1↓, STAT3↓,
720- Bor,    High Concentrations of Boric Acid Trigger Concentration-Dependent Oxidative Stress, Apoptotic Pathways and Morphological Alterations in DU-145 Human Prostate Cancer Cell Line
- in-vitro, Pca, DU145
ROS↑, TumCG↓, Apoptosis↑,
1450- Bos,  Cisplatin,    3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells
- in-vitro, Pca, DU145
ROS↑, MMP↓, Casp↑, Apoptosis↑, Bax:Bcl2↑, TumCCA?, cycD1/CCND1↓, CDK4↓, P21↑, p27↑, NOTCH↓, ChemoSen↑,
5746- CA,    Caffeic acid hinders the proliferation and migration through inhibition of IL-6 mediated JAK-STAT-3 signaling axis in human prostate cancer
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
tumCV↓, ROS↑, TumCCA↑, Apoptosis↑, p‑MAPK↓, ERK↓, JNK↓, p38↓, IL6↓, JAK1↓, p‑STAT3↓, cycD1/CCND1↓, CDK1↓, BAX↑, Casp3↑, Bcl-2↓, TumCD↑,
2792- CHr,    Chrysin induces death of prostate cancer cells by inducing ROS and ER stress
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
DNAdam↑, TumCCA↑, MMP↓, ROS↑, lipid-P↑, ER Stress↑, UPR↑, PERK↑, eIF2α↑, GRP78/BiP↑, PI3K↓, Akt↓, p70S6↓, MAPK↑,
143- CUR,    Nonautophagic cytoplasmic vacuolation death induction in human PC-3M prostate cancer by curcumin through reactive oxygen species -mediated endoplasmic reticulum stress
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ER Stress↑, CHOP↑, GRP78/BiP↑, ROS↑, LC3II↑, eff↓, tumCV↓,
161- CUR,  MeSA,    Enhanced apoptotic effects by the combination of curcumin and methylseleninic acid: potential role of Mcl-1 and FAK
- in-vitro, BC, MDA-MB-231 - in-vitro, Pca, DU145
Mcl-1↑, Mcl-1↓, MPT↑, AIF↑, chemoPv↑, Apoptosis↑, ROS↑, FAK↓, STAT3↓, NF-kB↓,
117- CUR,    Increased Intracellular Reactive Oxygen Species Mediates the Anti-Cancer Effects of WZ35 via Activating Mitochondrial Apoptosis Pathway in Prostate Cancer Cells
- in-vivo, Pca, RM-1 - in-vivo, Pca, DU145
ROS↑, tumCV↓, Apoptosis↑, TumCCA↑, Ca+2↑, eff↓, ER Stress↑,
118- CUR,    Curcumin analog WZ35 induced cell death via ROS-dependent ER stress and G2/M cell cycle arrest in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
ROS↑, Bcl-2↓, PARP↑, cDC2↓, CycB/CCNB1↓, MDM2↓, eff↓, eIF2α↑, ATF4↑, CHOP↑, ER Stress↑, TumCCA↑,
134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, ROS↑, Trx1↓, TumCG↓, eff↓, TXNIP↑,
132- CUR,    Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells
- in-vitro, Pca, PC3
TumCCA↑, ROS↑, TumAuto↑, UPR↑, ER Stress↑, Casp3↑, Casp9↑, Casp12↑, PARP↑, other↝, GRP78/BiP↑, PDI↑, eIF2α↑, other↝,
159- CUR,    Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment
- in-vitro, Pca, DU145
ROS↑, p‑Jun↑, p‑p38↑, TumAuto↑, Casp8↑, Casp9↑, Akt↓, ERK↓, p38↓,
462- CUR,    Curcumin promotes cancer-associated fibroblasts apoptosis via ROS-mediated endoplasmic reticulum stress
- in-vitro, Pca, PC3
Bcl-2↓, MMP↓, cl‑Casp3↑, BAX↑, BIM↑, p‑PARP↑, PUMA↑, p‑P53↑, ROS↑, p‑ERK↑, p‑eIF2α↑, CHOP↑, ATF4↑,
1869- DCA,    Dichloroacetate induces autophagy in colorectal cancer cells and tumours
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29
LC3II↑, ROS↑, mTOR↓, MCT1↓, NADH:NAD↓, NAD↑, TumAuto↑, lactateProd↓, LDH↑,
4456- DFE,    Induction of apoptosis and cell cycle arrest by ethyl acetate fraction of Phoenix dactylifera L. (Ajwa dates) in prostate cancer cells
- in-vitro, Pca, PC3
TumCD↑, MMP↓, mt-ROS↑, Apoptosis↑, TumCCA↑,
5386- docx,  AsP,    Co-delivery of docetaxel and palmitoyl ascorbate by liposome for enhanced synergistic antitumor efficacy
- vitro+vivo, Liver, HepG2 - in-vitro, BC, MCF-7 - in-vitro, Pca, PC3
Dose↝, ROS↑, eff↑, eff↑,
5495- EP,    Irreversible electroporation in focal therapy for prostate cancer: current status and future directions
- Review, Pca, NA
Ca+2↑, ATP↓, mtDam↑, ROS↑, CellMemb↑,
1955- GamB,    Gambogic acid inhibits thioredoxin activity and induces ROS-mediated cell death in castration-resistant prostate cancer
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
ROS↑, Apoptosis↑, Ferroptosis↑, Trx↓, eff↑, TrxR↓, Dose∅, MMP↓, eff↑, Casp↑, NADPH↓, TrxR↓, ChemoSen↑, AR↓,
1958- GamB,    Gambogenic acid induces apoptosis and autophagy through ROS-mediated endoplasmic reticulum stress via JNK pathway in prostate cancer cells
- in-vitro, Pca, NA - in-vivo, NA, NA
AntiCan↑, TumCP↓, TumAuto↑, eff↑, JNK↑, ROS↑, ER Stress↑, eff↓, TumCG↓,
2060- GamB,    Gambogenic acid induces apoptosis and autophagy through ROS-mediated endoplasmic reticulum stress via JNK pathway in prostate cancer cells
- in-vitro, Pca, NA
TumCP↓, TumAuto↑, eff↑, ROS↑, ER Stress↑, JNK↑,
4637- HT,    Comparative Cytotoxic Activity of Hydroxytyrosol and Its Semisynthetic Lipophilic Derivatives in Prostate Cancer Cells
- in-vitro, Nor, RWPE-1 - in-vitro, Pca, LNCaP - in-vitro, Pca, 22Rv1 - in-vitro, Pca, PC3
selectivity↑, TumCMig↓, p‑Akt↓, ROS↑, CSCs↓, CD44↓, TumCP↓,
4639- HT,    Hydroxytyrosol Induces Apoptosis, Cell Cycle Arrest and Suppresses Multiple Oncogenic Signaling Pathways in Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TumCP↓, selectivity↑, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, P21↑, p27↑, Apoptosis↑, Casp↑, cl‑PARP↑, Bax:Bcl2↑, p‑Akt↓, p‑STAT3↓, NF-kB↓, AR↓, ROS↑, *BioAv↓, *toxicity∅,
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↓,
1721- Lyco,  RES,  VitC,    Lycopene, resveratrol, vitamin C and FeSO4 increase damage produced by pro-oxidant carcinogen 4-nitroquinoline-1-oxide in Drosophila melanogaster: Xenobiotic metabolism implications.
- in-vitro, Pca, PC3 - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Liver, HepG2
ROS↑,
4803- Lyco,    Enhanced cytotoxic and apoptosis inducing activity of lycopene oxidation products in different cancer cell lines
- in-vitro, Pca, PC3 - in-vitro, BC, MCF-7 - in-vitro, Melanoma, A431 - in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
tumCV↓, GSH↓, MDA↑, ROS↑, Apoptosis↑,
582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, Ferroptosis↑, ROS↑, TumCG↓, Iron↑, GPx4↓,
526- MF,    Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Pca, HeLa - vitro+vivo, Melanoma, B16-BL6 - in-vitro, Nor, HEK293
TumCG↓, Ca+2↑, selectivity↑, *Ca+2∅, ROS↑, HSP70/HSPA5↑, AntiCan↑,
4946- PEITC,    Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, TumAuto↑, ROS↑, OXPHOS↓, ATP↓, selectivity↑, ETC↓, eff↓, eff↓, BAX↑,
4950- PEITC,    Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential
- vitro+vivo, Pca, PC3
MMP↓, Cyt‑c↑, Smad1↑, Diablo↑, ROS↑,
5186- PEITC,    Phenethyl Isothiocyanate inhibits STAT3 activation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
TumCP↓, TumCCA↑, STAT3↓, p‑JAK2↓, eff↓, TumCCA↑, AR↓, ROS↑,
1985- PTL,    KEAP1 Is a Redox Sensitive Target That Arbitrates the Opposing Radiosensitive Effects of Parthenolide in Normal and Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Nor, PrEC - in-vivo, NA, NA
ROS↑, NADPH↑, RadioS↑, radioP↑, Trx↓, *ox-Keap1↑, ox-Keap1↓, rd-Keap1↑, *NRF2↑, NRF2∅, NF-kB↓,
1987- PTL,  Rad,    A NADPH oxidase dependent redox signaling pathway mediates the selective radiosensitization effect of parthenolide in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Nor, PrEC
selectivity↑, RadioS↑, ROS↑, *ROS∅, NADPH↑, Trx↓, PI3K↑, Akt↑, p‑FOXO3↓, SOD2↓, Catalase↓, radioP↑, *NADPH∅, *GSH↑, *GSH/GSSG↑, *NRF2↑,
66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt/(β-catenin)↓, PSA↓, VEGF↓, PARP↑, Casp3↑, Casp9↑, DR5↑, ROS⇅, Shh↓, P53↑, P21↑, EGFR↓, TumCCA↑, ROS↑, miR-21↓, TumCP↓, selectivity↑, PDGF↓, EGF↓, TNF-α↓, VEGFR2↓, mTOR↓, cMyc↓, MMPs↓, GRP78/BiP↑, CHOP↑,
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
PrxI∅, PrxII∅, *toxicity↓, ROS↓, ROS↑, ROS∅, chemoP↑, PrxII↑, i-H2O2↓,
89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
PI3K/Akt↓, cMET↓, Casp3↑, Casp9↑, MMP↓, ChemoSen↑, ROS↑,
90- QC,  HP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
ROS↑, cl‑Casp3↑, cl‑PARP↑, miR-21↓, PDCD4↑, TAC↑, tumCV↓, TumCI↓,
88- QC,  PacT,    Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production
- vitro+vivo, Pca, PC3
ROS↑, ER Stress↑, TumCP↓, Apoptosis↑, TumCCA↑, TumCMig↓, GRP78/BiP↑, CHOP↑, TumCG↓,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,

Showing Research Papers: 1 to 50 of 67
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 67

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Fenton↑, 1,   Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH∅, 1,   GSTP1/GSTπ↓, 1,   i-H2O2↓, 1,   HO-1↓, 1,   HO-2↑, 1,   Iron↑, 1,   ox-Keap1↓, 1,   rd-Keap1↑, 1,   lipid-P↑, 1,   MDA↓, 1,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 1,   NRF2∅, 1,   OXPHOS↓, 1,   PrxI∅, 1,   PrxII↑, 1,   PrxII∅, 1,   ROS↓, 3,   ROS↑, 49,   ROS⇅, 1,   ROS∅, 1,   mt-ROS↑, 1,   SOD↓, 1,   SOD↑, 2,   SOD1↑, 1,   SOD2↓, 1,   TAC↑, 1,   Trx↓, 3,   Trx1↓, 1,   TrxR↓, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 2,   EGF↓, 2,   ETC↓, 1,   FGFR1↓, 1,   MMP↓, 11,   MPT↑, 1,   mtDam↑, 2,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   cMyc↓, 3,   GlucoseCon∅, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 2,   lactateProd∅, 1,   LDH↑, 2,   LDHA↓, 1,   NAD↑, 1,   NADH:NAD↓, 1,   NADPH↓, 1,   NADPH↑, 2,   PI3K/Akt↓, 1,   PKM2↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 2,   Apoptosis↑, 20,   Bak↑, 1,   BAX↓, 1,   BAX↑, 9,   Bax:Bcl2↑, 2,   Bcl-2↓, 8,   Bcl-xL↓, 2,   BIM↑, 2,   Casp↑, 5,   Casp12↑, 1,   Casp3↓, 1,   Casp3↑, 8,   cl‑Casp3↑, 4,   proCasp3↓, 1,   Casp8↑, 2,   Casp9↑, 6,   cl‑Casp9↑, 1,   Cyt‑c↑, 5,   Diablo↑, 1,   DR5↑, 3,   FasL↑, 1,   Ferroptosis↑, 2,   JNK↓, 1,   JNK↑, 5,   MAPK↓, 2,   MAPK↑, 2,   p‑MAPK↓, 1,   Mcl-1↓, 1,   Mcl-1↑, 1,   MCT1↓, 1,   MDM2↓, 2,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,   p27↑, 3,   p38↓, 2,   p38↑, 2,   p‑p38↑, 1,   PDCD4↑, 1,   PUMA↑, 1,   TumCD↑, 3,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 2,   miR-21↑, 1,   other↝, 2,   p‑pRB↓, 1,   tumCV↓, 8,  

Protein Folding & ER Stress ⓘ

CHOP↑, 7,   eIF2α↑, 3,   p‑eIF2α↑, 1,   ER Stress↑, 10,   GRP78/BiP↑, 6,   HSP70/HSPA5↓, 2,   HSP70/HSPA5↑, 2,   PERK↑, 1,   UPR↑, 3,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3B-II↑, 1,   LC3II↑, 2,   p62↓, 1,   p62↑, 2,   TumAuto↑, 7,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   P53↑, 4,   p‑P53↑, 2,   PARP↓, 1,   PARP↑, 3,   p‑PARP↑, 3,   cl‑PARP↑, 3,   proPARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 3,   CDK2↓, 1,   CDK2↑, 1,   CDK4↓, 2,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 6,   cycE/CCNE↓, 1,   cycE1↓, 1,   P21↑, 6,   TumCCA?, 1,   TumCCA↑, 16,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   cDC2↓, 1,   cFos↓, 1,   cFos↑, 1,   cMET↓, 1,   CSCs↓, 2,   EMT↓, 2,   ERK↓, 3,   ERK↑, 1,   p‑ERK↑, 1,   FGF↓, 1,   p‑FOXO3↓, 1,   p‑GSK‐3β↓, 1,   IGFBP3↑, 1,   p‑Jun↑, 1,   mTOR↓, 3,   p‑mTOR↑, 1,   NOTCH↓, 2,   PI3K↓, 3,   PI3K↑, 1,   RAS↓, 1,   Shh↓, 2,   STAT3↓, 3,   p‑STAT3↓, 3,   TumCG↓, 7,   TumCG↑, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↑, 3,   FAK↓, 2,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 2,   PDGF↓, 2,   RIP3↑, 1,   p‑RIP3↑, 1,   Smad1↑, 1,   TGF-β↓, 1,   TSP-1↑, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 9,   TXNIP↑, 1,   uPA↓, 1,   uPAR↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 2,   EGFR↓, 2,   Hif1a↑, 2,   PDI↑, 1,   VEGF↓, 2,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

CellMemb↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 3,   JAK1↓, 2,   p‑JAK2↓, 1,   NF-kB↓, 5,   p65↓, 1,   PSA↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 3,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   Dose↝, 1,   Dose∅, 2,   eff↓, 13,   eff↑, 8,   RadioS↑, 3,   selectivity↓, 1,   selectivity↑, 13,  

Clinical Biomarkers ⓘ

AR↓, 3,   CRP↓, 1,   EGFR↓, 2,   HER2/EBBR2↓, 1,   IL6↓, 3,   LDH↑, 2,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   chemoP↑, 2,   chemoPv↑, 1,   radioP↑, 2,   TumVol↓, 1,   TumW↓, 2,  
Total Targets: 237

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   GSH/GSSG↑, 1,   ox-Keap1↑, 1,   NRF2↑, 2,   ROS∅, 3,  

Core Metabolism/Glycolysis ⓘ

NADPH∅, 1,  

Cell Death ⓘ

Apoptosis∅, 1,  

Migration ⓘ

Ca+2∅, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 11

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
8 Curcumin
7 Quercetin
5 Selenite (Sodium)
4 Vitamin C (Ascorbic Acid)
3 Alpha-Lipoic-Acid
3 Radiotherapy/Radiation
3 Resveratrol
3 Gambogic Acid
3 Phenethyl isothiocyanate
3 Sulforaphane (mainly Broccoli)
2 Silver-NanoParticles
2 Apigenin (mainly Parsley)
2 Berberine
2 Docetaxel
2 HydroxyTyrosol
2 Lycopene
2 Magnetic Fields
2 Parthenolide
2 VitK3,menadione
1 Glucose
1 Allicin (mainly Garlic)
1 Metformin
1 Ashwagandha(Withaferin A)
1 Baicalein
1 borneol
1 Boron
1 Boswellia (frankincense)
1 Cisplatin
1 Caffeic acid
1 Chrysin
1 methylseleninic acid
1 Melatonin
1 Silymarin (Milk Thistle) silibinin
1 Dichloroacetate
1 Date Fruit Extract
1 Ascorbyl Palmitate
1 Electrical Pulses
1 lambertianic acid
1 immunotherapy
1 benzo(a)pyrene
1 doxorubicin
1 Hyperoside
1 Paclitaxel
1 salinomycin
1 Spermidine
1 erastin
1 Selenium
1 Thymoquinone
1 Urolithin
1 Vitamin K2
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:22  Cells:%  prod#:%  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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