Resveratrol Cancer Research Results

RES, Resveratrol: Click to Expand ⟱
Features: polyphenol
Found in red grapes and products made with grapes.
Resveratrol is a polyphenol compound found in various plant species, including grapes, berries, and peanuts.
• Anti-inflammatory effects, Antioxidant effects:
- Antiplatelet aggregation for stroke prevention
- BioAvialability use piperine
- some sources may use Japanese knotweed roots (Reynoutria Japonica - root) as source which might contain Emodin (laxative)
-known as Nrf2 activator, both in cancer and normal cells. Which raises controversity of use in ROS↑ therapies. Interestingly there are reports of NRF2↑ and ROS↑ in cancer cells. This raises the question of if it is a chemosensitizer. However other reports indicate NRF2 droping with Res, indicating it maybe a chemosenstizer.
- RES is also considered to be them most effective natural SIRT1↑ -activating compound (STACs).

However, in the presence of certain metals, such as copper or iron, resveratrol can undergo a process called Fenton reaction, which can lead to the generation of reactive oxygen species (ROS). The pro-oxidant effects of resveratrol are often observed at high concentrations, typically above 50-100 μM, and in the presence of certain metals or other pro-oxidant agents. In contrast, the antioxidant effects of resveratrol are typically observed at lower concentrations, typically below 10-20 μM.

Clinical trials have used doses ranging from 150 mg to 5 grams per day. Lower doses (< 1 g/day) are often well-tolerated, but higher doses might be necessary for therapeutic effects and can be associated with side effects.

-Note half-life 1-3 hrs?.
BioAv poor: min 5uM/L required for chemopreventive effects, but 25mg Oral only yeilds 20nM. co-administration of piperine
Pathways:
- usually induce ROS production in cancer cells, while reducing ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓,
- Lowers AntiOxidant defense in Cancer Cells: NRF2(typically increased), TrxR↓**, SOD">SOD↓, GSH↓ Catalase↓ HO1↓(wrong direction), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑">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↓, RhoA↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- 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 /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD133↓, CD24↓, β-catenin↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK,
- 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- & context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation Resveratrol can act as a pro-oxidant in cancer cells while functioning as an antioxidant in normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction and apoptosis follow ROS elevation in cancer cells
3 SIRT1 / AMPK axis ↑ AMPK; context-dependent SIRT1 modulation ↑ SIRT1 / ↑ AMPK Driver Metabolic stress signaling Resveratrol modulates energy-sensing pathways affecting survival and metabolism
4 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Secondary Growth and anabolic inhibition Downregulation of growth signaling contributes to cytostasis and apoptosis sensitization
5 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of survival and inflammatory transcription NF-κB inhibition contributes to reduced proliferation and invasion
6 Cell cycle regulation ↑ G1/S or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling disruption
7 HIF-1α / VEGF axis ↓ HIF-1α; ↓ VEGF ↔ minimal Secondary Anti-angiogenic pressure Interference with hypoxia-driven adaptation and angiogenesis


Scientific Papers found: Click to Expand⟱
2206- AgNPs,  RES,    ENHANCED EFFICACY OF RESVERATROL-LOADED SILVER NANOPARTICLE IN ATTENUATING SEPSIS-INDUCED ACUTE LIVER INJURY: MODULATION OF INFLAMMATION, OXIDATIVE STRESS, AND SIRT1 ACTIVATION
- in-vivo, Nor, NA
*hepatoP↑, AgNPs + RV treatment significantly reduced pro-inflammatory cytokines, NF-κB activation, presepsin, PCT, 8-OHDG, and VEGF levels compared with the CLP group, indicating attenuation of sepsis-induced liver injury.
*Inflam↓,
*NF-kB↓,
*VEGF↓,
*SIRT1↑, Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects.
*ROS↓, alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation.
*Dose↝, 30 mg/kg of AgNPs + RV was given intraperitoneally to the rats
*Catalase↑, AgNPs + RV treatment exhibited a robust effect in bolstering CAT activity
*MDA↓, AgNPs + RV treatment effectively ameliorates sepsis-induced oxidative stress and inflammation in rat livers by reducing MDA, MPO, and NO levels
*MPO↓,
*NO↓,
*ALAT↓, AgNPs + RV effectively reduced the ALT and AST levels, returning them to values similar to those observed in the Sham group
*AST↓,
*antiOx↑, corroborates the antioxidant potential of RV and AgNPs observed in earlier studies

2578- ART/DHA,  RES,    Synergic effects of artemisinin and resveratrol in cancer cells
- in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa
Dose↝, The combination of ART and Res exhibited the strongest anticancer effect at the ratio of 1:2 (ART to Res).
TumCMig↓, combination of the two drugs also markedly reduced the ability of cell migration
Apoptosis↑, Apoptosis analysis showed that combination of ART and Res significantly increased the apoptosis and necrosis rather than use singly
necrosis↑,
ROS↑, ROS levels were elevated by combining ART with Res.
eff↑, the data suggested that the IC50 of the combination of ART and Res is lower than that of each drug used alone.

6027- CGA,  CUR,  EGCG,  QC,  RES  Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol
- Review, Nor, NA
*ROS↓, polyphenols have similar chemical and biological properties in that they can act as antioxidants and exert the anticancer effects via cell signaling pathways involving their reactive oxygen species (ROS)-scavenging activity.
ROS↑, These polyphenols may also act as pro-oxidants under certain conditions, especially at high concentrations.

16- CP,  RES,    Resveratrol inhibits the hedgehog signaling pathway and epithelial-mesenchymal transition and suppresses gastric cancer invasion and metastasis
- in-vitro, GC, SGC-7901
HH↓, decrease in Gli-1, Snail and N-cadherin expression, and an increase in E-cadherin expression in the resveratrol and cyclopamine group compared
Gli1↓,
EMT↓, suggesting that resveratrol inhibited the Hh pathway and EMT, as did cyclopamine.
N-cadherin↓,
E-cadherin↑,
Snail↓,
TumCI↓, suppress invasion and metastasis in gastric cancer in vitro.
TumMeta↓, Resveratrol and cyclopamine inhibits the metastasis and invasion of SGC-7901 cells

5780- CRMs,  HCAs,  RES,  Sper,  ASA  Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential
- Review, Var, NA
*OS↑, The permanent or periodic reduction of calorie intake without malnutrition (caloric restriction and fasting) is the only strategy that reliably extends healthspan in mammals including non-human primates.
*AntiAge↑, CRMs will become part of the pharmacological armamentarium against aging and age-related cardiovascular, neurodegenerative, and malignant diseases.
*cardioP↑,
*neuroP↑,
AntiCan↑,
*TNF-α↓, In healthy humans, CR also decreases the levels of circulating tumor necrosis factor-α
*Weight↓, In obese humans, CR promotes significant weight loss and improves general health
*BP↓, Figure 1
*Inflam↓,
*Insulin↓,
*ROS↓,
*AMPK↑,
*mTOR↓,
*SIRT1↑, Resveratrol and Other SIRT1 Activators
CRM↑, Figure2: HCA, Resveratrol, Spermidine, Aspirin, Berberine, EGCG, QC, etc

5791- CRMs,  HCA,  NAD,  Sper,  RES  Caloric Restriction Mimetics in Nutrition and Clinical Trials
- Review, Nor, NA
*Dose↝, Among others, glycolytic inhibitors (e.g., D-allulose, D-glucosamine), hydroxycitric acid, NAD+ precursors, polyamines (e.g., spermidine), polyphenols (e.g., resveratrol, dimethoxychalcones, curcumin, EGCG, quercetin) and salicylic acid
*Glycolysis↓, CRM candidates were suspected among inhibitors of glycolysis,

4881- CUR,  SFN,  RES,  EGCG,  Lyco  An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↑, natural Nrf2 activators include curcumin, sulforaphane (SF), kahweol, resveratrol, garlic oganosulfur compounds, zerumbone, epigallocatechin-3-gallate, carnosol, cinnamonyl-based compounds, lycopene, and cafestol
*antiOx↑, these chemopreventive agents can activate the antioxidants, phase II detoxification factors, and transducers, and protect the cells from carcinogenic exposure

5397- CUR,  SFN,  RES,  EGCG,  Ash  Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential
- Review, Var, NA
CSCs↓, curcumin, sulforaphane, resveratrol, EGCG, genistein, quercetin, parthenolide, berberine, and withaferin A. Collectively, these compounds suppress CSC self-renewal,

3862- CUR,  RES,    The metalloproteinase ADAM10: A useful therapeutic target?
- Review, AD, NA
*SIRT1↑, Therefore, the Sirt1 activators curcumin and resveratrol are tested for their clinical impact on ADAM10 expression in AD.
*ADAM10↑,

3748- CUR,  RES,  Hup,  Riv,  Gala  Natural acetylcholinesterase inhibitors: A multi-targeted therapeutic potential in Alzheimer's disease
- Review, AD, NA
*AChE↓, natural phytocompounds such as Curcumin, Varenicline, Huperrtzine, Resveratrol, and Cycloastrageno have received FDA approval to treat Alzheimer's disease
*Inflam↓, Anti-amyloidogenic, anti-inflammatory, anti-ChE, anti – secretase
*Aβ↓, Prevent cognitive impairment and associated oxidative stress by reducing plaque formation
*cognitive↑,
*ROS↓,

128- CUR,  RES,    Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer
- in-vivo, Pca, NA
lipid-P↓,
chemoPv↑, Amongst various chemo-preventive agents, phytochemicals especially curcumin and resveratrol in combination have shown great potential in combating cancer
GSH↑, However, supplementation with curcumin and resveratrol resulted in significant increase in the reduced glutathione levels in DMAB treated rats.
SOD↑, Similar trends were noticed in the enzyme activities of super-oxide disumutase and glutathione-s- transferase in DMAB treated rats, when supplemented with combination of phytochemicals.
GSTs↑,
glucose↓, combined treatment of curcumin and resveratrol resulted in appreciable moderation in the uptakes and turnover of glucose in the prostates of DMAB treated rats

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↑, curcumin and resveratrol promote ROS production and induce apoptosis in LNCaP and PC-3.
Trx1↓, Melatonin and silibinin did not change the basal redox state in LNCaP and these compounds even caused a further TRX1 reduction in PC-3 cells.
TumCG↓, Melatonin and silibinin inhibit cell growth while curcumin and resveratrol induce apoptosis in prostate cancer cell
eff↓, NAC prevents curcumin-induced apoptosis
TXNIP↑, Resveratrol decreases TRX1 by increasing TXNIP mRNA levels in PC-3 cells.

182- CUR,  RES,  GI,    Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
p38↓,
MKP5↑, MKP5 was up-regulated by curcumin and inhibited TNFa- and IL-1b-stimulated p38 phosphorylation, COX-2 up-regulation, NFjB activation and cytokine production in E-PZ cells
TNF-α↓,
COX2↓,
NF-kB↓,

872- CUR,  RES,    New Insights into Curcumin- and Resveratrol-Mediated Anti-Cancer Effects
- in-vitro, BC, TUBO - in-vitro, BC, SALTO
TumCP↓,
tumCV↓,
p62↓, reduced by Cur
p62↑, accumulated by Res
TumAuto↑, Cur only
TumAuto↓, Res only
ROS↑, increased ROS with Res
ROS↓, decreased ROS with Cur or combination
CHOP↑, strongly upregulated by the curcumin/resveratrol combination

1383- CUR,  BBR,  RES,    Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases
- Review, NA, NA
GSK‐3β↝,
ROS↑, BBB increased ROS production by decreasing c-MYC expression

685- EGCG,  CUR,  SFN,  RES,  GEN  The “Big Five” Phytochemicals Targeting Cancer Stem Cells: Curcumin, EGCG, Sulforaphane, Resveratrol and Genistein
- Analysis, NA, NA
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Apoptosis↑,
Nanog↓,
cMyc↓,
OCT4↓,
Snail↓,
Slug↓,
Zeb1↓,
TCF↓,

4664- GEN,  CUR,  RES,  EGCG,  SFN  Targeting cancer stem cells by nutraceuticals for cancer therapy
- Review, Var, NA
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
other↝, Because chemotherapy and radiotherapy cannot effectively remove CSCs
eff↑, Curcumin and EGCG combination attenuated the CD44+ cell population via inhibition of pSTAT3 and retaining the crosstalk between STAT3 and NF-κB in breast cancer cells [233]
CD44↓,
p‑STAT3↓,

166- GEN,  EGCG,  RES,  CUR,    Common botanical compounds inhibit the hedgehog signaling pathway in prostate cancer
- in-vivo, Pca, NA
HH↓, The four compounds, which inhibited Hedgehog signaling in both cell assays (genistein, curcumin, EGCG, and resveratrol), are potentially cheaper and safer alternatives to cyclopamine
Gli1↓, Three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA concentration but not Gli reporter activity.

1534- LT,  Api,  EGCG,  RES,    Plant polyphenol induced cell death in human cancer cells involves mobilization of intracellular copper ions and reactive oxygen species generation: a mechanism for cancer chemopreventive action
- in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, PC, Bxpc-3
TumCP↓,
Apoptosis↑,
eff↓, cell death is prevented to a significant extent by cuprous chelator neocuproine and reactive oxygen species scavengers
*toxicity↑, normal breast epithelial cells, cultured in a medium supplemented with copper, become sensitized to polyphenol-induced growth inhibition.
Dose?, apigenin at 5uM promoted growth in MCF10A cells and PC3 cancer cells. This could be because polyphenols at lower concentrations are known to be associated with cell proliferation [21], while behaving as prooxidants at high concentrations
eff↓, Apigenin- and luteolin-induced antiproliferation and apoptosis in cancer cells is inhibited by cuprous chelator but not by iron and zinc chelators
eff↓, EGCG and resveratrol, similar to that of the flavones luteolin and apigenin, also involves the mobilization of endogenous copper and consequent prooxidant effect leading to cell death.

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↑, We propose that the basal levels of the XM's enzymes in the ST cross interacted with a putative pro-oxidant activity of the compounds added to the pro-oxidant effects of 4-NQO.

4701- PTS,  RES,    Targeting cancer stem cells and signaling pathways by resveratrol and pterostilbene
- Review, Var, NA
CSCs↓, Resveratrol and pterostilbene target CSCs
E-cadherin↑, " E-cadherin, # NF-jB, # EMT-associated molecules (Twist1,vimentin)
NF-kB↓,
EMT↓,
GRP78/BiP↓, GRP78
CD133↓, CD133
COX2↓, COX-2,
β-catenin/ZEB1↓,
NOTCH↓, Notch

4703- PTS,  RES,    Pterostilbene and resveratrol: Exploring their protective mechanisms against skin photoaging - A scoping review
- NA, Nor, NA
*AntiAge↑, resveratrol shows significant promise in combating skin photoaging, pterostilbene is still in the early exploration phases.
*eff↑, Pterostilbene demonstrates potential to outperform resveratrol
*Inflam↓, well known for properties, such as anti-aging, anti-inflammatory, anti-melanogenesis, and anti-cancer
*AntiCan↑,
*ROS↓, Pterostilbene significantly prevented UVB-induced reduction in cell viability and increased reactive oxygen species (ROS) production
*Catalase↑, pterostilbene significantly increased gene expression of catalase (CAT)
*GSR↑, glutathione reductase (GSR), heme oxygenase-1 (HMOX-1) and NAD(P)H quinone dehydrogenase 1 (NQO1);
*HO-1↑,
*NAD↑,
*NQO1↑,
*SOD↑, while significantly increasing glutathione disulfide (GSSH), SOD, nuclear Nrf2,
*NRF2↑,

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
cJun↑, Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
AR↓,

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

3080- RES,    Resveratrol: A miraculous natural compound for diseases treatment
- Review, Var, NA
SIRT1↑, PC12 cells Aβ‐induced apoptosis Inline graphic Feng et al. (2013) SIRT‐1↑ ROCK1↓
ROCK1↓,
AMPK↑, SAMP8 mice SIRT‐1 and AMPK↑
*lipid-P↓, Sprague–Dawley rats Lipid peroxidation↓ Aβ aggregation in hippocampus↓
Aβ↓,
COX2↓, RSV decreases the prostaglandins (PGs) expression by inhibition of COX‐2 enzyme
angioG↓, suggest that RSV may act as an anticancer agent to inhibit angiogenesis through affecting hypoxia‐inducible factor‐1 alpha (HIF‐1α) and vascular endothelial growth factor (VEGF) in different cancer cells in vitro
Hif1a↓,
VEGF↓,

3073- RES,    Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy
- in-vitro, Nor, NA
*NLRP3↓, inhibits NLRP3 inflammasome-derived IL-1β secretion and pyroptosis in macrophages.
*mtDam↓, Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage
*p38↑, Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol.

3074- RES,    Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer
- Review, BC, NA
NLRP3↓, The active form of Resveratrol (RSV) inhibits NLRP3-mediated inflammasome activation by Sirt1 (SIRT1) / p53-dependent cellular aging.
SIRT1↑,

3075- RES,  Rad,    The Protection Effect of Resveratrol Against Radiation-Induced Inflammatory Bowel Disease via NLRP-3 Inflammasome Repression in Mice
- in-vivo, Nor, NA
*SIRT1↑, Here we show that resveratrol, the activator of Sirt1, could alleviate the bowel inflammation induced by irradiation and the expression of Sirt1 is consistent with the inflammation level.
*radioP↑,
*NLRP3↓, against radiation-induced inflammatory bowel disease via NLRP-3 inflammasome repression in mice and supports Sirt1 as a potential biomarker
*Weight↑, The weight of C57BL / 6 mice in each group treated with resveratrol gradually increased from the 6th day after irradiation, while the weight of C57BL/6 mice in the irradiation group still showed a downward trend.
*IL1β↓, Resveratrol Inhibited the Expression of IL-1β and NLRP-3 in Spleen and Thymus

3076- RES,    Resveratrol for targeting the tumor microenvironment and its interactions with cancer cells
- Review, Var, NA
IL6↓, A dose-dependent reduction of IL-6 by resveratrol led to attenuation of matrix metalloproteinases (MMPs), including MMP2 and MMP9
MMPs↓,
MMP2↓,
MMP9↓,
BioAv↓, The most important weakness of the usual form of resveratrol is its low absorption in the intestine and its low bioavailability
Half-Life↑, some covers such as liposomes and micelles also can facilitate absorption and increase half-life
BioAv↑, another study showed that carboxymethyl chitosan can increase bioavailability by more than 3.5 times
Dose↝, low concentrations of resveratrol (lower than 50 uM) cause no remarkable toxicity for normal cells, while higher concentrations are associated with increased oxidative injury
angioG↓, It is suggested that inhibition of STAT3, IL-10, and a reduction of vascular endothelial growth factor (VEGF) by resveratrol is involved in the suppression of macrophages and reduction of invasion and angiogenesis
IL10↓,
VEGF↓,
NF-kB↓, Inhibition of NF-kB by resveratrol can attenuate the expression of COX-2.
COX2↓,
SIRT1↑, Activation of Sirt-1 by resveratrol has a role in the suppression of NF-kB
Wnt↓, Resveratrol has also been shown that inhibit the Wnt/C-Myc pathway too
cMyc↓,
STAT3↓, Resveratrol has been shown that attenuate the expression of STAT3 through reduction of IL-6 level
PTEN↑, Downregulation of miR-17, miR-20a and miR-106b by resveratrol can activate PTEN, which leads to suppression of PI3K and induction of apoptosis in cancer cells
ROS↑, Resveratrol can trigger NOX5-induced ROS, leading to the induction of DNA damage and cancer cells senescence
RadioS↑, The combination of radiation and resveratrol has shown that has a synergic effect for stimulation of ROS production and induction of senescence in non-small cell lung carci- noma
Hif1a↓, Resveratrol can inhibit HIF-1α and its downstream proteins, including E-cadherin and vimentin
E-cadherin↓,
Vim↓,
angioG↓, Furthermore, resveratrol inhibits angiogenesis markers and tumor growth through the inhibition of HIF-1a

3077- RES,    Resveratrol attenuates matrix metalloproteinase-9 and -2-regulated differentiation of HTB94 chondrosarcoma cells through the p38 kinase and JNK pathways
- in-vitro, Chon, HTB94
MMP2↓, We found that resveratrol significantly inhibited MMP-2 and MMP-9, and induced the expression of type II collagen and sex-determining region Y-box (SOX)-9 and the production of sulfated proteoglycans in HTB94 chondrosarcoma cells.
MMP9↓,
SOX9↑,
MMPs↓,
p‑p38↑, Phosphorylation of p38 was increased and phosphorylation of c-Jun N-terminal kinase (JNK) was inhibited by resveratrol
p‑JNK↓,
NF-kB↓, Moreover, resveratrol reduced lung adenocarcinoma cell metastasis by suppressing heme oxygenase (HO)-1-mediated nuclear factor (NF)-κB pathway activation and subsequently downregulated the expression of MMPs.
HO-1↓, Resveratrol inhibited the transcription-activator function of HO-1 and subsequently MMP-2 and MMP-9 expression in human lung cancer cells as well.

3078- RES,    The Effects of Resveratrol on Prostate Cancer through Targeting the Tumor Microenvironment
- Review, Pca, NA
*ROS↓, RSV appears to be both pro- and anti-oxidant, depending on the circumstances [76]. In non-cancer tissues, RSV serves as an antioxidant [77], and therefore RSV can exert a beneficial effect on a wide variety of issues, including neuronal [78], anti-in
ROS↑, However, to cancer cells with low pH environments due to the Warburg Effect, RSV shows more pro-oxidant characteristics.
DNAdam↑, RSV can induce cancer cell death by inducing ROS accumulation, which subsequently leads to oxidative DNA damage and apoptosis
Apoptosis↑,
Hif1a↑, Wang et al. demonstrated that RSV-enhanced cancer cell death is due to the upregulation of HIF1α, which enhances ROS concentration in the TME beyond the limit for survival
Casp3↑, superoxide can activate caspases 9 and 3, and subsequently promote the release of cytochrome C
Casp9↑,
Cyt‑c↑,
Dose↝, It is important to note that low concentration of RSV can serve as a pro-oxidant that favors cell survival, and pro-apoptotic effects occur only at relatively higher RSV concentrations to stimulate superoxide production.
MMPs↓, inhibitory effect of RSV on MMPs has been shown in many cancer types, and RSV is capable of inhibiting both MMP-2 and MMP-9
MMP2↓,
MMP9↓,
EMT↓, RSV can restore the epithelial phenotype of the mesenchymal cells and inhibit the expression of EMT-related markers
E-cadherin↑, RSV can inhibit EMT by up- and downregulating E-cadherin and N-cadherin, respectively, in prostate cancer cells.
N-cadherin↓,
AR↓, RSV can repress AR function by inhibiting AR transcriptional activity

3079- RES,    Therapeutic role of resveratrol against hepatocellular carcinoma: A review on its molecular mechanisms of action
- Review, Var, NA
angioG↓, Resveratrol suppresses angiogenesis and metastatic markers to reverse cancer spread.
TumMeta↓,
ChemoSen↑, Resveratrol chemosensitizes chemotherapy and synergizes anti-cancer phytochemicals.
NADPH↑, Both in vitro and in vivo studies indicates that resveratrol enhances various redox enzymes activity, especially nicotinamide adenine dinucleotide phosphate (NADPH)
SIRT1↑, resveratrol effectively modulates both the cytokine and chemokine profiles in immune and endothelial cells by the upregulation of sirtuin-1 (SIRT1)
NF-kB↓, suppression of NF-κB and prevention of the activation of NOD-like receptor family (Nrf) pyrin domain containing-3 inflammasome [
NLRP3↓,
Dose↝, The optimal dose of resveratrol being around 150 mg per day is considered safe by all means.
COX2↓, Cox2 ↓; MMP9 ↓
MMP9↓,
PGE2↓, Cox1 and 2; PGE2↓
TIMP1↑, Resveratrol suppresses the PMA-induced MMP activity in HepG2 cell line, while it also upregulates tissue inhibitor proteins of MMP, namely, TIMP1 and TIMP2, in dose-dependent manner
TIMP2↑,
Sp1/3/4↓, Resveratrol mitigates the expression of SP-1 by inhibiting both phosphorylation of JNK1/2 and expression of urokinase-type plasminogen activator in Huh-7 cell line
p‑JNK↓,
uPAR↓,
ROS↓, Resveratrol attenuates the excessive ROS production and inflammatory cytokine, IL-6, and CXCR4 receptor expression by downregulating Gli-1 expression.
CXCR4↓,
IL6↓,
Gli1↓,
*ROS↓, redox imbalance may be attenuated by resveratrol via downregulating ROS production and simultaneously inducing antioxidant enzymes, GST, SOD, CAT and GPx activities in the cells
*GSTs↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*lipid-P↓, [72] observed that resveratrol treatment not only reduces lipid peroxidation but also increases GSH and GST serum levels in CCl4-treated rats as compared to the CCl4-control animals
*GSH↑,
eff↑, Resveratrol, in combination with thymoquinone (TQ), has been demonstrated to provide a synergistic antiproliferative efficacy against HCC cell lines as reported by Ismail et al.
eff↑, Curcumin, a potential anticancer phytochemical, in combination with resveratrol has been reported to trigger synergistic apoptotic effects against Hepa1–6 cells
eff↑, berberine in combination with resveratrol lowers the cell viability and cell adhesion. At low concentration, berberine significantly induces cell death while resveratrol inhibits cell migration in HepG2 cells

3072- RES,    Resveratrol ameliorates glioblastoma inflammatory response by reducing NLRP3 inflammasome activation through inhibition of the JAK2/STAT3 pathway
- in-vitro, GBM, LN229 - in-vitro, GBM, U87MG
tumCV↓, RSV significantly inhibited cell viability in GBM cell lines LN-229 and U87-MG.
TumCP↓, it inhibited the proliferation and invasive migration ability of GBM cells, while promoting apoptosis.
TumCMig↓,
Apoptosis↑,
NLRP3↓, RSV inhibited the over-activation of the inflammasome NLRP3 through the JAK2/STAT3 signaling pathway.
JAK2↓, by inhibiting the activation of the JAK2/STAT3 signaling pathway.
STAT3↓,
IL1β↓, RSV indeed decreased the levels of inflammasome NLRP3 and its downstream IL-1β, IL-18, IL-6, and TNFα.
IL18↓,
IL6↓,
TNF-α↓,
Inflam↓, partly mediated by improving the inflammatory state of GBM

3081- RES,    Resveratrol and p53: How are they involved in CRC plasticity and apoptosis?
- Review, CRC, NA
NF-kB↓, At 5 µM, resveratrol repressed inflammation (NF-κB), CRC progression (FAK, Ki-67, MMP-9, CXCR4) and CSC production (CD44, CD133, ALDH1).
FAK↓, Inhibition of FAK signaling pathway and thereby attenuation of invasion by resveratrol
Ki-67↓,
MMP9↓,
CSCs↓,
CD44↓,
CD133↓,
ALDH1A1↓,
EMT↓, resveratrol inhibits not only EMT but also enhances CRC cells‘ sensitivity to the standard chemotherapeutic drug 5-FU
ChemoSen↑,
Hif1a↓, Suppression of HIF-1α using β1-integrin receptors through resveratrol, thereby inhibition of inflammation
ITGB1↓,
Inflam↓,

3082- RES,    Resveratrol Ameliorates the Malignant Progression of Pancreatic Cancer by Inhibiting Hypoxia-induced Pancreatic Stellate Cell Activation
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vivo, NA, NA
VEGF↓, Furthermore, our in vivo studies revealed that the administration of RSV to LSL-KrasG12D/+, Trp53fl/+, and Pdx1-Cre (KPC) mice by gastric perfusion could significantly suppress VEGF-A, SDF-1, IL-6, alpha-smooth muscle actin (α-SMA), and HIF-1α expres
CXCL12↓,
IL6↓,
α-SMA↓,
Hif1a↓,
TumCI↓, RSV Suppresses Pancreatic Cancer Cell Invasion and EMT Induced by Hypoxia
EMT↓,

3083- RES,    Resveratrol suppresses breast cancer cell invasion by inactivating a RhoA/YAP signaling axis
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
YAP/TEAD↓, we demonstrate that resveratrol decreases the expression of YAP target genes
Rho↓, Strikingly, we also demonstrate that resveratrol inactivates RhoA, leading to the activation of Lats1 and induction of YAP phosphorylation.
FAK↓, REV decreases breast cancer cell invasion by inhibiting FAK,44 Rac and Cdc4245 activities
MMP9↓, REV has been shown to downregulate MMP-9 expression
ChemoSen↑, REV enhances the anticancer effects of doxorubicin in breast cancer cells
RAS↓, we reported that REV suppresses LPA-induced EGF receptor activation and subsequent inhibition a Ras/RhoA/ROCK signaling in ovarian cancer cells
ROCK1↓,
TumCI↓, REV may be used to reduce invasion and metastasis of breast cancer cells to improve outcomes for this devastating disease.
TumMeta↓,

3084- RES,    Resveratrol inhibits the proliferation of estrogen receptor-positive breast cancer cells by suppressing EZH2 through the modulation of ERK1/2 signaling
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D
TumCP↓, Resveratrol inhibited the proliferation and colony formation in ER-positive breast cancer cells and downregulated EZH2 through inhibition of phospho-ERK1/2.
EZH2↓,
p‑ERK↓,

3085- RES,    Resveratrol interrupts Wnt/β-catenin signalling in cervical cancer by activating ten-eleven translocation 5-methylcytosine dioxygenase 1
- in-vitro, Cerv, NA
TET1↑, After treating cervical cancer cells with Resveratrol (RES), we found that TET1 expression was elevated and Wnt/β-catenin pathway activity was suppressed.
Wnt↓,
β-catenin/ZEB1↓,

3086- RES,    Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
TET1↑, Res upregulated the 5hmC and TET1 levels and downregulated the 5mC level.
TumCMig↓, Res also inhibited the migration and invasion of PCa cells
TumCI↓,
TIMP2↑, promoted the demethylation of TIMP2 and TIMP3 to upregulate their expressions, and suppressed the expressions of MMP2 and MMP9.
TIMP3↑,
MMP2↓,
MMP9↓,

3087- RES,    Resveratrol cytotoxicity is energy-dependent
- Review, Var, NA
OXPHOS↓, The inhibition of the oxidative phosphorylation (OXPHOS) pathway appears to be the molecular mechanism of resveratrol.
eff↝, This review suggests that investigating a possible complex relationship between caloric intake and the differential effects of resveratrol on OXPHOS may be justified.
eff↑, A low-calorie diet accompanied by significant levels of resveratrol might modify cellular bioenergetics, which could impact cellular viability and enhance the anti-cancer properties of resveratrol.

3088- RES,    Notch signaling mediated repressive effects of resveratrol in inducing caspasedependent apoptosis in MCF-7 breast cancer cells
- in-vitro, BC, MCF-7
NOTCH1↓, findings further displayed a significant reduction in cell viability in resveratrol-treated MCF-7 cancer cells, which were concomitantly related to the downregulation of Notch-1, Jagged-1, and DLL4.
BAX↑, expression of Bax, Bcl-2, cyclin D1, CDK4, p21, and caspase-3 activation.
CDK4↝,
Casp3↑,
P21↑,

3089- RES,    The Role of Resveratrol in Cancer Therapy
- Review, Var, NA
angioG↓, resveratrol plays a role in inhibiting the expression of MMP (mainly MMP-9) [174,175,176,177] and angiogenesis markers such as VEGF, EGFR or FGF-2
VEGF↓,
EGFR↓,
FGF↑,
TumCMig↓, Resveratrol reduced the phorbo-12-myristate 13-acetate (PMA)-induced migration and invasion ability of liver cancer HepG2 and Hep3B cells.
TumCI↓,
TIMP1↑, resveratrol up-regulated TIMP-1 protein expression and down-regulated MMP-9 activity, while the activities of MMP-2 and MMP-9 were decreased,
MMP2↓,
MMP9↓,
NF-kB↓, via down-regulating the expression of NF-κB,
Hif1a↓, It has been reported that resveratrol suppresses the expression of VEGF and HIF-1α in human ovarian cancer cells via abrogating the activation of the PI3K/Akt and MAPK signaling pathways
PI3K↓,
Akt↓,
MAPK↓,
EMT↓, Many studies have shown that resveratrol suppresses the development of tumor invasion and metastasis through inhibiting signaling pathways associated with EMT
AR↓, Resveratrol suppressed prostate cancer growth via down-regulating the androgen receptor (AR) expression in the TRAMP model of prostate cancer

3071- RES,    Resveratrol and Its Anticancer Effects
- Review, Var, NA
chemoPv↑, In this review, the effects of resveratrol are emphasized on chemopreventive, therapeutic, and anticancer.
SIRT1↑, RSV can directly activate Sirt1 expression and induce autophagy independently or dependently on the mammalian target of rapamycin (mTOR)
Hif1a↓, RSV suppresses tumor angiogenesis by inhibiting HIF-1a and VEGF protein
VEGF↓,
STAT3↓, RSV effectively prevents cancer by inhibiting STAT3 expression
NF-kB↓, also has an inhibitory effect on antiapoptotic mediators such as NF-kB, COX-2, phosphatidylinositol 3-kinase (PI3K), and mTOR (52).
COX2↓,
PI3K↓,
mTOR↓,
NRF2↑, Activation of the Nrf2/antioxidant response element (ARE) pathway by endogenous or exogenous stimuli under normal physiological conditions has the potential to inhibit cancer and/or cancer cell survival, growth, and proliferation
NLRP3↓, RSV downregulates the NLRP3 gene by activating the Sirt1 protein, thereby inducing autophagy
H2O2↑, RSV mediates cytotoxicity in cancer cells by increasing intracellular hydrogen peroxide (H2O2) and oxidative stress levels that will cause cell death
ROS↑,
P53↑, RSV activates p53, increases the expression of PUMA and BAX
PUMA↑,
BAX↑,

3070- RES,    Resveratrol inhibits tumor progression by down-regulation of NLRP3 in renal cell carcinoma
- in-vitro, RCC, ACHN - in-vitro, RCC, 786-O - in-vivo, NA, NA
TumCP↓, We found that RSV inhibited tumor cells proliferation, migration and invasion and increased apoptosis of RCC either in vivo or in vitro.
TumCMig↓,
TumCI↓,
Apoptosis↑,
NLRP3↓, RSV significantly down-regulated expressions of NLRP3 and its downstream genes.

3069- RES,    Resveratrol Inhibits NLRP3 Inflammasome-Induced Pyroptosis and miR-155 Expression in Microglia Through Sirt1/AMPK Pathway
- in-vitro, Nor, N9
*antiOx↑, antioxidant, anti-carcinogenic, anti-obesity, anti-aging, anti-inflammatory, immunomodulatory properties.
*Inflam↓,
*ROS↓, Our results demonstrated that resveratrol inhibits LPS- and ATP-activated NLRP3 inflammasome and protects microglial cells upon oxidative stress, proinflammatory cytokine production, and pyroptotic cell death resulting from inflammasome activation.
*NF-kB↓, resveratrol inhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and activates AMPK/Sirt1 pathways.
*AMPK↑,
*SIRT1↑,
*miR-155↓, Furthermore, our results indicated that resveratrol downregulated inflammasome-induced miR-155 expression
*NLRP3↓, To sum up, our results suggest that resveratrol suppresses the NLRP3 inflammasome and miR-155 expression through AMPK and Sirt1 pathways in microglia.

3068- RES,    Resveratrol decreases the expression of genes involved in inflammation through transcriptional regulation
- in-vitro, lymphoma, U937
p65↓, In our study, RESV treatment significantly decreased p65 expression and reduced the activities of the antioxidant enzymes SOD2, PRX2, CAT, and TRX.
SOD2↓,
Prx↓,
Catalase↓,
Trx↓,
TNF-α↓, (i.e., TNF-α, IL-8, and MCP-1), whereas a reduction in the protein levels of these cytokines was observed in the presence of RESV.
IL8↓,
MCP1↓,
SIRT1↑, a trend of increased SIRT1 activity in the presence of RESV was observed, which may be due to the low dose of RESV used

3067- RES,    Proteomic Profiling Reveals That Resveratrol Inhibits HSP27 Expression and Sensitizes Breast Cancer Cells to Doxorubicin Therapy
- in-vitro, BC, MCF-7
Apoptosis↑, Consistently, we demonstrated that resveratrol induces apoptosis in MCF-7 cells
MMP↓, Apoptosis was associated with a significant increase in mitochondrial permeability transition, cytochrome c release in cytoplasm, and caspases -3 and -9 independent cell death.
Cyt‑c↑,
Casp3↑,
Casp9↑,
HSP27↓, We propose that potential modulation of HSP27 levels using natural alternative agents, as resveratrol, may be an effective adjuvant in breast cancer therapy

3066- RES,    Resveratrol triggers ER stress-mediated apoptosis by disrupting N-linked glycosylation of proteins in ovarian cancer cells
GSK‐3β↑, resveratrol suppressed the hexosamine biosynthetic pathway and interrupted protein glycosylation through GSK3β activation
Akt↓, Akt attenuation in response to resveratrol.
CHOP↑, Resveratrol-mediated disruption of protein glycosylation induced cellular apoptosis as indicated by the up-regulation of GADD153, followed by the activation of ER-stress sensors (PERK and ATF6α).
ER Stress↑,
PERK↑,
ATF6↑,
UPR↑, Disruption of protein glycosylation causes the accumulation of aberrant of proteins in the endoplasmic reticulum (ER) which in turn activates unfolded protein responses (UPR) in the ER, leading to severe stressful conditions
GlucoseCon↓, Previous studies have shown that resveratrol (RSV) impairs glucose consumption via Akt/GLUT1 axis in cancer [

3065- RES,    Resveratrol-induced cytotoxicity in human Burkitt's lymphoma cells is coupled to the unfolded protein response
- in-vitro, lymphoma, NA
UPR↑, treatment with RES lead to the activation of all 3 branches of the UPR
IRE1↑, with early splicing of XBP-1 indicative of IRE1 activation, phosphorylation of eIF2α consistent with ER resident kinase (PERK) activation, activating transcription factor 6 (ATF6) splicing
p‑eIF2α↑,
PERK↑,
ATF6↑,
GRP78/BiP↑, increase in expression levels of the downstream molecules GRP78/BiP, GRP94 and CHOP/GADD153 in human Burkitt's lymphoma Raji and Daudi cell lines.
GRP94↑,
CHOP↑,
GADD34↑, RES induces a pathway initiated by phosphorylation of eIF2α and followed by the upregulation of GADD34 and ATF4.
ATF4↑,
XBP-1↑, RES increased XBP-1 expression both in Raji and in Daudi cells
Ca+2↑, RES was found to significantly increase cytosolic Ca2+
ER Stress↑, RES was able to induce ER stress and activated all 3 branches of the UPR.

3064- RES,    Resveratrol Suppresses Cancer Cell Glucose Uptake by Targeting Reactive Oxygen Species–Mediated Hypoxia-Inducible Factor-1α Activation
- in-vitro, CRC, HT-29 - in-vitro, BC, T47D - in-vitro, Lung, LLC1
FDG↓, Resveratrol mildly decreased cell content and more pronouncedly suppressed 18F-FDG uptake in Lewis lung carcinoma, HT-29 colon, and T47D breast cancer cells.
ROS↓, Resveratrol also decreased intracellular ROS in patterns that closely paralleled 18F-FDG uptake.
Hif1a↓, HIF-1α protein was markedly reduced by resveratrol,
GLUT1↓, 50uM, Resveratrol Inhibits Glut-1 Expression and Lactate Production
lactateProd↓,


Showing Research Papers: 1 to 50 of 170
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 170

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GSH↑, 1,   GSTs↑, 1,   H2O2↑, 1,   HO-1↓, 1,   lipid-P↓, 1,   NRF2↑, 1,   OXPHOS↓, 1,   Prx↓, 1,   ROS↓, 3,   ROS↑, 9,   SOD↑, 1,   SOD2↓, 1,   Trx↓, 1,   Trx1↓, 1,  

Mitochondria & Bioenergetics ⓘ

MKP5↑, 1,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 2,   CRM↑, 1,   FDG↓, 1,   glucose↓, 1,   GlucoseCon↓, 1,   lactateProd↓, 1,   NADPH↑, 1,   SIRT1↑, 6,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 8,   BAX↑, 2,   Bcl-2↓, 1,   Casp3↑, 3,   Casp9↑, 2,   Cyt‑c↑, 2,   GADD34↑, 1,   p‑JNK↓, 2,   MAPK↓, 1,   necrosis↑, 1,   p38↓, 1,   p‑p38↑, 1,   PUMA↑, 1,   survivin↓, 1,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9↑, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

cJun↑, 1,   EZH2↓, 1,   other↝, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ATF6↑, 2,   CHOP↑, 3,   p‑eIF2α↑, 1,   ER Stress↑, 2,   GRP78/BiP↓, 1,   GRP78/BiP↑, 1,   GRP94↑, 1,   HSP27↓, 1,   IRE1↑, 1,   PERK↑, 2,   UPR↑, 2,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

p62↓, 1,   p62↑, 1,   TumAuto↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↝, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD133↓, 2,   CD44↓, 2,   CSCs↓, 4,   EMT↓, 7,   p‑ERK↓, 1,   FGF↑, 1,   Gli1↓, 3,   GSK‐3β↑, 1,   GSK‐3β↝, 1,   HH↓, 2,   mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 2,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 3,   p‑STAT3↓, 1,   TCF↓, 1,   TumCG↓, 1,   Wnt↓, 2,  

Migration ⓘ

Ca+2↑, 1,   CXCL12↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 3,   FAK↓, 2,   ITGB1↓, 1,   Ki-67↓, 1,   MMP2↓, 5,   MMP9↓, 8,   MMPs↓, 3,   N-cadherin↓, 2,   Rho↓, 1,   ROCK1↓, 2,   Slug↓, 1,   Snail↓, 2,   TET1↑, 2,   TIMP1↑, 2,   TIMP2↑, 2,   TIMP3↑, 1,   TumCI↓, 6,   TumCMig↓, 5,   TumCP↓, 5,   TumMeta↓, 3,   TXNIP↑, 1,   uPAR↓, 1,   Vim↓, 1,   Zeb1↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 7,   Hif1a↑, 1,   VEGF↓, 5,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 6,   CXCR4↓, 1,   IL10↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 4,   IL8↓, 1,   Inflam↓, 2,   JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 8,   p65↓, 1,   PGE2↓, 1,   TNF-α↓, 3,  

Protein Aggregation ⓘ

Aβ↓, 1,   NLRP3↓, 5,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 3,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   Dose?, 1,   Dose↝, 4,   eff↓, 4,   eff↑, 6,   eff↝, 1,   Half-Life↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 3,   EGFR↓, 1,   EZH2↓, 1,   IL6↓, 4,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 2,  
Total Targets: 163

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 3,   GPx↑, 1,   GSH↑, 1,   GSR↑, 1,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 8,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 2,   Glycolysis↓, 1,   NAD↑, 1,   SIRT1↑, 5,  

Cell Death ⓘ

p38↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

miR-155↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 5,   NF-kB↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   ADAM10↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   NLRP3↓, 3,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   Dose↝, 2,   eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   OS↑, 1,   radioP↑, 1,   toxicity↑, 1,   Weight↓, 1,   Weight↑, 1,  
Total Targets: 51

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

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