EGCG (Epigallocatechin Gallate) Cancer Research Results

EGCG, EGCG (Epigallocatechin Gallate): Click to Expand ⟱
Features:
EGCG (Epigallocatechin Gallate) is found in green tea. 100 times more effective than Vitamin C and 25 times more effective than Vitamin E at protecting cells from damage associated with oxidative stress.
EGCG Epigallocatechin Gallate (Green Tea) -Catechin
Summary:
1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.
2. Poor bioavailability: taking EGCG capsules without food was better.
3. Cancer dosage 4g/day (2g twice per day)? with curcumin may help (another ref says 700–2100 mg/d)
4. EGCG is susceptible to oxidative degradation.
5. “As for the pH level, the acidic environments enhance the stability of EGCG”.
6. “EGCG may enhance nanoparticle uptake by tumor cells”
7. Might be iron chelator (removing iron from cancer cells)
8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.
9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.
10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).
11. EGCG mediated ROS formation can upregulate CTR1 expression via the ERK1/2/NEAT1 pathway, which can increase the intake of chemotherapeutic drugs such as cisplatin in NSCLC cells and act as a chemosensitizer [58]
12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.
13. EGCG is an ENOX2 inhibitor.
14. Nrf2 activator in both cancer and normal cells. This example of lung cancer show both directions in different cell lines, but both toward optimim level.
Biological activity, EGCG has been reported to exhibit a range of effects, including:
    Antioxidant activity: 10-50 μM
     Anti-inflammatory activity: 20-50 μM
     Anticancer activity: 50-100 μM
     Cardiovascular health: 20-50 μM
     Neuroprotective activity: 10-50 μM

Drinking a cup (or two cups) of green tea (in which one might ingest roughly 50–100 mg of EGCG from brewed tea) generally results in peak plasma EGCG concentrations in the range of approximately 0.1 to 0.6 μM.

With higher, supplement-type doses (e.g., oral doses in the 500 mg–800 mg range that are sometimes studied for clinical benefits), peak plasma concentrations in humans can reach the low micromolar range, often reported around ~1–2 μM and in some cases up to 5 μM.

Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.
In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.

-Peak plasma concentration roughly 1 to 2 hours after oral ingestion.
-Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.

Supplemental EGCG
Dose (mg)   ≈ Peak Plasma EGCG (µM)
~50 mg          ≈ 0.1–0.3 µM
~100 mg         ≈ 0.2–0.6 µM
~250 mg         ≈ 0.5–1.0 µM
~500 mg         ≈ 1–2 µM
~800 mg or higher  ≈ 1–5 µM

50mg of EGCG in 1g of matcha tea(1/2 teaspoon)

Studies on green tea extracts have employed doses roughly equivalent to 300–800 mg/day of EGCG. Excessive doses can cause liver toxicity in some cases.

Methods to improve bioavailability
-Lipid-based carriers or nanoemulsions
-Polymer-based nanoparticles or encapsulation
-Co-administration with ascorbic acid (vitamin C)
-Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan) -Using multiple smaller doses rather than one large single dose.
-Taking EGCG on an empty stomach or under fasting conditions, or aligning dosing with optimal pH conditions in the GI tract, may improve its absorption.(acidic environment is generally more favorable for its stability and absorption).
– EGCG is more stable under acidic conditions. In the stomach, where the pH is typically around 1.5 to 3.5, EGCG is less prone to degradation compared to the more neutral or basic environments of the small intestine.
- At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.
– Although the stomach’s acidic pH helps maintain EGCG’s stability, most absorption occurs in the small intestine, where the pH is closer to neutral.
– To counterbalance the inherent instability in the intestine, strategies such as co-administration of pH-modifying agents (like vitamin C) are sometimes used. These agents help to maintain a slightly acidic environment in the gut microenvironment, potentially improving EGCG stability during its transit and absorption.
– The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.

-Note half-life 3–5 hours.
- low BioAv 1%? despite its limited absorption, it is rapidly disseminated throughout the body
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Does NOT Lower AntiOxidant defense in Cancer Cells: NRF2↑, TrxR↓**, SOD, GSH Catalase HO1 GPx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, 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↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, Notch↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective(possible damage at high dose), CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation EGCG can act as a pro-oxidant in cancer cells (often metal-catalyzed) while functioning as an antioxidant in normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial stress and apoptosis follow ROS elevation in cancer cells
3 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of survival and inflammatory transcription NF-κB inhibition explains chemosensitization and reduced survival signaling
4 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Secondary Reduced growth and anabolic signaling AKT/mTOR inhibition contributes to growth suppression and stress responses
5 MAPK stress signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-activated apoptosis signaling MAPK activation often follows ROS increase and supports apoptotic signaling
6 Cell cycle regulation ↑ G1 or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling disruption rather than direct CDK inhibition
7 HIF-1α / VEGF hypoxia–angiogenesis axis ↓ HIF-1α; ↓ VEGF ↔ minimal Secondary Anti-angiogenic pressure EGCG interferes with hypoxia-driven tumor adaptation
8 NRF2 antioxidant response ↑ NRF2 (adaptive, often insufficient) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 reflects response to redox perturbation rather than a kill mechanism


Scientific Papers found: Click to Expand⟱
639- EGCG,    Immunomodulatory Effects of Green Tea Catechins and Their Ring Fission Metabolites in a Tumor Microenvironment Perspective
- Review, NA, NA
TIMP3↑, MMP2↓, MMP9↓,
21- EGCG,    Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in mice
- in-vivo, Liver, NA
HH↓, PTCH1↓, Smo↓, Gli1↓, CD44↓, β-catenin/ZEB1↓,
22- EGCG,    Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics
- in-vitro, PC, CD133+ - in-vitro, PC, CD44+ - in-vitro, PC, CD24+ - in-vitro, PC, ESA+
HH↓, Smo↓, PTCH1↓, PTCH2↓, Gli1↓, GLI2↓, Gli↓, Bcl-2↓, XIAP↓, Shh↓, survivin↓, Casp3↑, Casp7↑, CSCs↓, Nanog↓, cMyc↓, OCT4↓, EMT↓, Snail↓, Slug↓, Zeb1↓, TumCMig↓, TumCI↓, eff↑,
23- EGCG,    (-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cells
- in-vitro, Chon, SW1353 - in-vitro, Chon, CRL-7891
HH↓, Gli1↓, PTCH1↓, Bcl-2↓, BAX↑, TumCG↓,
24- EGCG,  GEN,  QC,    Targeting CWR22Rv1 prostate cancer cell proliferation and gene expression by combinations of the phytochemicals EGCG, genistein and quercetin
- in-vitro, Pca, 22Rv1
NQO1↑, P53↑, NQO2↑, chemoPv↑, TumCP↓, AR↓,
25- EGCG,  QC,    Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
COMT↓, TumCP↑, TumCCA↑, Apoptosis↑,
26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓, cl‑PARP↑, Casp7↑, IκB↓, Ki-67↓, VEGF↓, EGFR↓, FGF↓, TGF-β↓, TNF-α↓, SCF↓, Bax:Bcl2↑, NF-kB↓, chemoP↑, ChemoSen↑, TumVol↓,
637- EGCG,  CAP,    Cancer prevention trial of a synergistic mixture of green tea concentrate plus Capsicum (CAPSOL-T) in a random population of subjects ages 40-84
- Human, NA, NA
ENOX2↓,
638- EGCG,  MushCha,  MushReishi,    A Case of Complete and Durable Molecular Remission of Chronic Lymphocytic Leukemia Following Treatment with Epigallocatechin-3-gallate, an Extract of Green Tea
- Case Report, AML, NA
Remission↑,
665- EGCG,    Anticancer effects of epigallocatechin-3-gallate nanoemulsion on lung cancer cells through the activation of AMP-activated protein kinase signaling pathway
- in-vitro, NA, H1299
AMPK↑, TumCP↓, TumCMig↓, TumCI↓,
640- EGCG,    Epigallocatechin Gallate (EGCG) Is the Most Effective Cancer Chemopreventive Polyphenol in Green Tea
- in-vitro, CRC, HCT116 - in-vitro, Colon, SW480
TumCCA↑, Apoptosis↑,
641- EGCG,  Se,    Antioxidant effects of green tea
ROS↑, H2O2↑, ROS⇅,
642- EGCG,    Prooxidant Effects of Epigallocatechin-3-Gallate in Health Benefits and Potential Adverse Effect
ROS↑, H2O2↑, Apoptosis↑, Trx↓, TrxR↓, JNK↑, HO-1↑, Fenton↑,
643- EGCG,    New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate
- Analysis, NA, NA
H2O2↑, Fenton↑, PDGFR-BB↑, EGFR↓, VEGFR2↓, IGFR↓, Ca+2↑, NO↑, Sp1/3/4↓, NF-kB↓, AP-1↓, STAT1↓, STAT3↓, FOXO↓, mtDam↑, TumAuto↑,
644- EGCG,  Citrate,    Simple Approach to Enhance Green Tea Epigallocatechin Gallate Stability in Aqueous Solutions and Bioavailability: Experimental and Theoretical Characterizations
- Analysis, Nor, NA
*BioAv↑,
645- EGCG,    The Effect of Ultrasound, Oxygen and Sunlight on the Stability of (−)-Epigallocatechin Gallate
- Analysis, NA, NA
eff↑, pH↓,
646- EGCG,  PI,    Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice
- in-vivo, Nor, NA
*BioAv↑,
647- EGCG,    Food Inhibits the Oral Bioavailability of the Major Green Tea Antioxidant Epigallocatechin Gallate in Humans
- Human, Nor, NA
*BioAv↑,
693- EGCG,  CAP,  Phen,    Metabolite modulation of HeLa cell response to ENOX2 inhibitors EGCG and phenoxodiol
- in-vitro, Cerv, HeLa
ENOX2↓, TumCG↓,
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↓,
686- EGCG,    Prevention effect of EGCG in rat's lung cancer induced by benzopyrene
- in-vivo, Lung, NA
NF-kB↓, p50↓, Ki-67↓,
667- EGCG,    Anti-cancer effect of EGCG and its mechanisms
- Review, NA, NA
RPSA↓,
688- EGCG,  GEM,    Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial–Mesenchymal Transition: Enhanced Efficacy When Combined with Gemcitabine
- in-vitro, PC, NA
Zeb1↓, β-catenin/ZEB1↓, Vim↓, Akt↓, p‑IGFR↓, TumCG↓, TumCMig↓, TumCI↓,
689- EGCG,    EGCG inhibited bladder cancer SW780 cell proliferation and migration both in vitro and in vivo via down regulation of NF-κB and MMP-9
- vitro+vivo, Bladder, SW780
Casp8↑, Casp9↑, Casp3↑, BAX↑, PARP↑, TumVol↓, NF-kB↓, MMP9↓,
690- EGCG,    Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer
- in-vitro, Pca, NA
AR↓, miR-21↓, miR-330-5p↑, TumCG↓,
691- EGCG,    Preclinical Pharmacological Activities of Epigallocatechin-3-gallate in Signaling Pathways: An Update on Cancer
- Review, NA, NA
Apoptosis↑, necrosis↑, TumAuto↑, ERK↓, p38↓, NF-kB↓, VEGF↓,
692- EGCG,    EGCG: The antioxidant powerhouse in lung cancer management and chemotherapy enhancement
- Review, NA, NA
ROS↑, Apoptosis↑, DNAdam↑, CTR1↑, JWA↑, β-catenin/ZEB1↓, P53↑, Vim↓, VEGF↓, p‑Akt↓, Hif1a↓, COX2↓, ERK↓, NF-kB↓, Akt↓, Bcl-xL↓, miR-210↓,
687- EGCG,    Estrogen receptor-α36 is involved in epigallocatechin-3-gallate induced growth inhibition of ER-negative breast cancer stem/progenitor cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
ER-α36↓,
694- EGCG,    Matcha green tea (MGT) inhibits the propagation of cancer stem cells (CSCs), by targeting mitochondrial metabolism, glycolysis and multiple cell signalling pathways
- in-vitro, BC, MCF-7
Glycolysis↓, GAPDH↓, ROS↑, OCR↓, ECAR↓, mTOR↓, OXPHOS↓,
695- EGCG,  TFdiG,    The antioxidant and pro-oxidant activities of green tea polyphenols: a role in cancer prevention
- in-vitro, NA, HL-60
ROS↑, IronCh↑, Apoptosis↑,
936- EGCG,    Bioactivity-Guided Identification and Cell Signaling Technology to Delineate the Lactate Dehydrogenase A Inhibition Effects of Spatholobus suberectus on Breast Cancer
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
LDHA↓,
937- EGCG,    Metabolic Consequences of LDHA inhibition by Epigallocatechin Gallate and Oxamate in MIA PaCa-2 Pancreatic Cancer Cells
- in-vitro, Pca, MIA PaCa-2
lactateProd↓, Glycolysis↓, GlucoseCon↓, LDHA↓,
989- EGCG,  Citrate,    In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity
- in-vitro, HCC, NA - in-vivo, NA, NA
PFK↓, Glycolysis↓, lactateProd↓, GlucoseCon↓, TumCP↓, TumCCA↑, Casp3↑, cl‑PARP↑, Apoptosis↑, Casp8↑, Casp9↑, Cyt‑c↝, MMP↓, BAD↑, GLUT2↓, PKM2∅,
1012- EGCG,    Inhibition of beta-catenin/Tcf activity by white tea, green tea, and epigallocatechin-3-gallate (EGCG): minor contribution of H(2)O(2) at physiologically relevant EGCG concentrations
- in-vitro, Nor, HEK293
*H2O2↑, *β-catenin/ZEB1↓, *TCF-4↓,
20- EGCG,    Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer
- in-vivo, Liver, NA - in-vivo, Tong, NA
HH↓, Gli1↓, Smo↓, TNF-α↓, COX2↓, *antiOx↑, Hif1a↓, NF-kB↓, VEGF↓, STAT3↓, Bcl-2↓, P53↑, Akt↓, p‑Akt↓, p‑mTOR↓, EGFR↓, AP-1↓, BAX↑, ROS↑, Casp3↑, Apoptosis↑, NRF2↑, *H2O2↓, *NO↓, *SOD↑, *Catalase↑, *GPx↑, *ROS↓,
673- EGCG,    Iron Chelation Properties of Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Analysis on Tfr/Fth Regulations and Molecular Docking
- in-vitro, CRC, HT-29
IronCh↑, TfR1/CD71↑, FTH1↓,
668- EGCG,    The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer Treatment
- Review, BC, MCF-7 - Review, BC, MDA-MB-231
HER2/EBBR2↓, EGFR↓, mtDam↑, ROS↑, PI3K/Akt↓, P53↑, P21↑, Casp3↑, Casp9↑, BAX↑, PTEN↑, Bcl-2↓, hTERT/TERT↓, STAT3↓, TumCCA↑, Hif1a↓,
669- EGCG,    Epigallocatechin-3-gallate and cancer: focus on the role of microRNAs
- Review, NA, NA
Let-7↑, KRAS↓,
670- EGCG,    Epigallocatechin-3-gallate and its nanoformulation in cervical cancer therapy: the role of genes, MicroRNA and DNA methylation patterns
- Review, NA, NA
TumCCA↑, P53↑, ERK↓, EGFR↓, p‑ERK↑, VEGF↓, Hif1a↓, miR-203↓, miR-210↑,
671- EGCG,    The Epigenetic Modification of Epigallocatechin Gallate (EGCG) on Cancer
other↝,
672- EGCG,    Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer
- Review, NA, NA
DNMT1↓, HDAC↓, G9a↓, PRC2↓, DNMT3A↓, 67LR↓, Apoptosis↑, TumCCA↑,
684- EGCG,    Improving the anti-tumor effect of EGCG in colorectal cancer cells by blocking EGCG-induced YAP activation
- in-vitro, CRC, NA
eff↑, Akt↓, VEGFR2↓, STAT3↓, P53↓, Hippo↓, YAP/TEAD↑,
674- EGCG,    Biocompatible and biodegradable nanoparticles for enhancement of anti-cancer activities of phytochemicals
- Review, Var, NA
*BioEnh↑,
675- EGCG,    When Natural Compounds Meet Nanotechnology: Nature-Inspired Nanomedicines for Cancer Immunotherapy
- Review, Var, NA
*BioAv↑,
676- EGCG,  Chemo,    The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review
- Review, NA, NA
PI3k/Akt/mTOR↓, Apoptosis↑, ROS↑, TumAuto↑,
677- EGCG,    Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2 α /ATF4 and IRE1 α
- in-vitro, CRC, HT-29
ER Stress↑, GRP78/BiP↑, PERK↑, eIF2α↑, ATF4↑, IRE1↑, Apoptosis↑,
678- EGCG,    Cancer Prevention with Green Tea and Its Principal Constituent, EGCG: from Early Investigations to Current Focus on Human Cancer Stem Cells
other↑, TumMeta↓, YMcells↑, CSCs↓,
679- EGCG,  5-FU,    Epigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancer
- in-vitro, CRC, NA
NOTCH1↓, BMI1↓, SUZ12↓, EZH2↓, miR-34a↑, miR-200c↑, miR-145↑, CSCs↓,
680- EGCG,    Cancer preventive and therapeutic effects of EGCG, the major polyphenol in green tea
- Review, NA, NA
NF-kB↓, STAT3↓, PI3K↓, HGF/c-Met↓, Akt↓, ERK↓, MAPK↓, AR↓, Casp↑, Ki-67↓, PARP↑, Bcl-2↓, BAX↑, PCNA↓, p27↑, P21↑,
681- EGCG,    Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical models
- vitro+vivo, BC, NA
Casp3↑, Casp8↑, Casp9↑, TumAuto↑, Beclin-1↝, ATG5↝, GlucoseCon↓, lactateProd↓, ATP↝, HK2↓, LDHA↓, Hif1a↓, GLUT1↓, TumVol↓, VEGF↓,

Showing Research Papers: 101 to 150 of 174
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 174

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ENOX2↓, 2,   Fenton↑, 2,   H2O2↑, 3,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   OXPHOS↓, 1,   ROS↑, 8,   ROS⇅, 1,   Trx↓, 1,   TrxR↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 1,   IronCh↑, 2,   TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↝, 1,   MMP↓, 1,   mtDam↑, 2,   OCR↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 2,   ECAR↓, 1,   GAPDH↓, 1,   GlucoseCon↓, 3,   GLUT2↓, 1,   Glycolysis↓, 3,   HK2↓, 1,   lactateProd↓, 3,   LDHA↓, 3,   PFK↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2∅, 1,   RPSA↓, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 2,   Apoptosis↑, 12,   BAD↓, 1,   BAD↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 6,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 6,   Casp7↑, 2,   Casp8↑, 3,   Casp9↑, 4,   Cyt‑c↝, 1,   HGF/c-Met↓, 1,   Hippo↓, 1,   hTERT/TERT↓, 1,   JNK↑, 1,   JWA↑, 1,   MAPK↓, 1,   necrosis↑, 1,   p27↑, 1,   p38↓, 1,   survivin↓, 2,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   miR-145↑, 1,   miR-21↓, 1,   other↑, 1,   other↝, 1,   PRC2↓, 1,   YMcells↑, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   IRE1↑, 1,   NQO2↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↝, 1,   Beclin-1↝, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   DNMT3A↓, 1,   G9a↓, 1,   P53↓, 1,   P53↑, 5,   PARP↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 2,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CD44↓, 1,   CSCs↓, 3,   EMT↓, 2,   ERK↓, 4,   p‑ERK↑, 1,   FGF↓, 1,   FOXO↓, 1,   Gli↓, 1,   Gli1↓, 4,   HDAC↓, 1,   HH↓, 4,   IGFR↓, 1,   p‑IGFR↓, 1,   Let-7↑, 1,   miR-330-5p↑, 1,   miR-34a↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   Nanog↓, 2,   NOTCH1↓, 1,   OCT4↓, 2,   PI3K↓, 1,   PTCH1↓, 3,   PTCH2↓, 1,   PTEN↑, 1,   SCF↓, 1,   Shh↓, 1,   Smo↓, 3,   STAT1↓, 1,   STAT3↓, 5,   SUZ12↓, 1,   TCF↓, 1,   TumCG↓, 4,  

Migration ⓘ

67LR↓, 1,   AP-1↓, 2,   Ca+2↑, 1,   ER-α36↓, 1,   GLI2↓, 1,   Ki-67↓, 3,   KRAS↓, 1,   miR-200c↑, 1,   miR-203↓, 1,   MMP2↓, 1,   MMP9↓, 2,   Slug↓, 2,   Snail↓, 2,   TGF-β↓, 1,   TIMP3↑, 1,   TumCI↓, 3,   TumCMig↓, 3,   TumCP↓, 3,   TumCP↑, 1,   TumMeta↓, 1,   Vim↓, 2,   Zeb1↓, 3,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   EGFR↓, 5,   Hif1a↓, 5,   miR-210↓, 1,   miR-210↑, 1,   NO↑, 1,   PDGFR-BB↑, 1,   VEGF↓, 6,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

CTR1↑, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IκB↓, 1,   NF-kB↓, 8,   p50↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

pH↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 3,   COMT↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 3,   EGFR↓, 5,   EZH2↓, 1,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 1,   Ki-67↓, 3,   KRAS↓, 1,   SUZ12↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   Remission↑, 1,   TumVol↓, 3,  
Total Targets: 179

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   H2O2↓, 1,   H2O2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TCF-4↓, 1,  

Migration ⓘ

β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 4,   BioEnh↑, 1,  
Total Targets: 12

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#:73  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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