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↓, ITG">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⟱
1541- Api,  EGCG,    Prospective cohort comparison of flavonoid treatment in patients with resected colorectal cancer to prevent recurrence
- Human, NA, NA
OS↑, Among the flavonoid-treated patients with resected colon cancer (n = 14), there was no cancer recurrence and one adenoma developed
Remission↓,
Dose∅, The flavonoid- treated patients took a daily dose of 2 tablets of the flavonoid mixture[24] containing 10 mg apigenin and 10 mg epigallocatechin-gallate per tablet.

147- ATG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

3754- BBR,  CUR,  EGCG,  Hup,    Traditional Chinese medicinal herbs as potential AChE inhibitors for anti-Alzheimer’s disease: A review
*AChE↓, Berberine (9) has gained considerable attention due to its wide pharmacological potentials and several biological properties, such as acetylcholinesterase and butyrylcholinesterase inhibitory, antioxidant, monoamine oxidase oxidase,
*Aβ↓, amyloid-b peptide level-reducing, cholesterol- lowering and renoprotective activities
*LDL↓,
*RenoP↑,
*BChE↓,
*eff↑, Above all, the berberine-pyrocatechol hybrid (14) showed a strong AChE inhibitor activity (IC50 of 123 ± 3 nM) [34]
*BACE↓, Curcumin: inhibite the rBACE1 activity [42]. In addition, it has made good inhibitory effect on acetylcholinesterase activity
*AChE↓, EGCG promoted brain health, prevented AD progression, and inhibited the AChE activity [52,53].
*eff↑, EGCG could enhance the effect of huperzine A on inhibiting AChE.

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.

5792- CRMs,  HCA,  CUR,  EGCG,  GAR  Caloric restriction mimetics: natural/physiological pharmacological autophagy inducers
- Review, Nor, NA
*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice

4656- CUR,  EGCG,    Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signaling
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
CSCs↓, Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44) positive cell population.
CD44↓,
p‑STAT3↓, curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained.
NF-kB↓, Notably, curcumin is a potent inhibitor of NFκB
TumCI↓, Wound-healing assay revealed that curcumin and EGCG suppress cell invasiveness

5783- CUR,  EGCG,    The effects of tetrahydrocurcumin and green tea polyphenol on the survival of male C57BL/6 mice
- in-vivo, Nor, NA
*OS↑, Mice that started to receive diets containing TC (0.2%) at the age of 13 months had significantly longer average life spans (days, mean +/- SD) than control mice (797.6 +/- 151.2 vs.882 +/- 154.6, both n = 50, controls vs.

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,

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

146- CUR,  EGCG,    Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
P21↑, The protein expressions of p21 were significantly increased by the co-treatment of EGCG and curcumin, whereas it was not changed by the treatment with each individual compound.
TumCCA↑, treatments of EGCG and curcumin arrested both S and G2/M phases of PC3 cells.
TumCP↓, EGCG inhibited PC3 cell proliferation to 11.2 and 24.3% at 50 and 100 μM, respectively.
BioAv↓, While curcumin has versatile anticancer properties, its poor absorption and low bioavailability are the challenges for its developmentas chemopreventive agent (33). The low bioavailability of EGCG is also confirmed i

162- CUR,  EGCG,  SFN,    Shattering the underpinnings of neoplastic architecture in LNCap: synergistic potential of nutraceuticals in dampening PDGFR/EGFR signaling and cellular proliferation
- in-vitro, Pca, LNCaP
p‑PDGF↓, phosphorylation

2501- EGCG,    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
OS↑, first published case report of "spontaneous" recovery from secondary autoimmune hemolytic anemia in an adult.
Remission↑, In 2015, more than three years after the documented remission, the patient remains well at age 52.
eff↑, The timing of this second remission, shortly after an increase in dose of epigallocatechin-3-gallate to 4 g daily, is provocative, as is the concurrent use of curcumin.
Dose↝, He takes epigallocatechin-3-gallate (1200 mg) daily and maintains his self-directed lifestyle regimen.

2459- EGCG,    Epigallocatechin gallate inhibits human tongue carcinoma cells via HK2‑mediated glycolysis
- in-vitro, Tong, Tca8113 - in-vitro, Tong, TSCCa
EGFR↓, EGCG exposure substantially decreased EGF-induced EGF receptor (EGFR), Akt and ERK1/2 activation, as well as the downregulation of hexokinase 2 (HK2).
Akt↓,
ERK↓,
HK2↓,
GlucoseCon↓, EGCG dose-dependently inhibited the consumption of glucose (Fig. 2A and B, middle) and production of lactate
lactateProd↓,
Glycolysis↓, EGCG downregulates HK2 expression and decreases human tongue carcinoma cell glycolysis.

2561- EGCG,  ASA,    Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatment
- ex-vivo, Nor, NA
AntiAg↑, EGCG significantly reduced ADP- and COL-induced platelet aggregation in dose-dependent manner
eff↑, no further increase of bleeding risk by EGCG in the participants who were already taking other anti-platelet agents.
Half-Life↝, half-life of EGCG is approximately 3 hours
other∅, EGCG significantly inhibited the human platelet aggregation without any changes on P-selectin and PAC-1 expressions.

2562- EGCG,    Green Tea Epigallocatechin 3-Gallate Reduced Platelet Aggregation and Improved Anticoagulant Proteins in Patients with Transfusion-Dependent β-Thalassemia: A Randomized Placebo-Controlled Clinical Trial
- Trial, NA, NA
AntiAg↑, in vitro treatment of GTE (at least 1 mg EGCG equivalent) inhibited PLT aggregation in patients who were healthy and with thalassemia platelet-rich plasma (PRP),
other↝, The results indicated that there were no significant differences in PT and aPTT values between the placebo group and the two groups receiving GTE tablets (50 and 100 mg EGCG equivalent) at the same time points during the intervention.

2563- EGCG,    Cardioprotective effect of epigallocatechin gallate in myocardial ischemia/reperfusion injury and myocardial infarction: a meta-analysis in preclinical animal studies
- Review, NA, NA
cardioP↑, EGCG significantly improves cardiac function, serum myocardial injury enzyme, and oxidative stress levels in MIRI animal models
ROS↑,
AntiAg↑, EGCG can inhibit platelet aggregation induced by U46619, collagen, arachidonic acid, and toxic carotenoids and shear force-induced platelet adhesion dose-dependently by suppressing PLCγ2 and tyrosine phosphorylation
eff↑, What’s more, its combination with common antiplatelet therapeutic agents, aspirin (ASA), clopidogrel (CPD), and tiglitazarol (TCG), did not further inhibit platelet aggregation resulting in bleeding complications
COX1↓, EGCG inhibits platelet activation by inhibiting microsomal cyclooxygenase-1 activity in platelets

2992- EGCG,    Effects of Epigallocatechin-3-Gallate on Matrix Metalloproteinases in Terms of Its Anticancer Activity
- Review, Var, NA
AP-1↓, MMPs have binding sites for at least one transcription factor of AP-1, Sp1, and NF-κB, and EGCG can downregulate these transcription factors through signaling pathways mediated by reactive oxygen species
Sp1/3/4↓,
NF-kB↓,
ERK↓, EGCG can also decrease nuclear ERK, p38, heat shock protein-27 (Hsp27), and β-catenin levels, leading to suppression of MMPs’ expression.
P-gp↓,
HSP27↓,
β-catenin/ZEB1↓,
MMPs↓,
TNF-α↓, suppress the production of inflammatory cytokines such as TNFα and IL-1β.
IL1β↓,
MMP2↓, EGCG inhibited MMP2 secretion in glioblastoma cells.

2993- EGCG,    Tea polyphenols down-regulate the expression of the androgen receptor in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP
TumCG↓, EGCG, inhibited LNCaP cell growth and the expression of androgen regulated PSA and hK2 genes.
PSA↓,
HK2↓,
AR↓, decrease in androgen receptor protein with treatments of the tea polyphenols EGCG, GCG and theaflavins.
Sp1/3/4↓, Sp1 is the target for the tea polyphenols because treatments of EGCG decreased the expression, DNA binding activity and transactivation activity of Sp1 protein.

2994- EGCG,    Nano-Engineered Epigallocatechin Gallate (EGCG) Delivery Systems: Overcoming Bioavailability Barriers to Unlock Clinical Potential in Cancer Therapy
- Review, Var, NA
BioAv↓, Despite its therapeutic promise, clinical application is constrained by rapid metabolism, poor bioavailability, and inconsistent biodistribution.
NF-kB↓, EGCG modulates oncogenic pathways via NF-κB suppression, caspase activation, and MMP-9 downregulation, demonstrating efficacy across diverse cancer types.
Casp↑,
MMP9↑,
Sp1/3/4↑, marked decrease in Sp1 activity

3201- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*AntiCan↑, EGCG’s therapeutic potential in preventing and managing a range of chronic conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes
*cardioP↑,
*neuroP↑,
*BioAv↝, Factors such as fasting, storage conditions, albumin levels, vitamin C, fish oil, and piperine have been shown to affect plasma concentrations and the overall bioavailability of EGCG
*BioAv↓, Conversely, bioavailability is reduced by processes such as air oxidation, sulfation, glucuronidation, gastrointestinal degradation, and interactions with Ca2+, Mg2+, and trace metals,
*BioAv↓, EGCG’s oral bioavailability is generally low, with marked differences observed across species, for example, bioavailability rates of 26.5% in CF-1 mice and just 1.6% in Sprague Dawley rats
*Dose↝, plasma concentrations exceeded 1 μM only when doses of 1 g or higher were administered.
*Half-Life↝, Specifically, a dose of 1600 mg yielded a Cmax of 3392 ng/mL (range: 130–3392 ng/mL), with peak levels observed between 1.3 and 2.2 h, AUC (0–∞) values ranging from 442 to 10,368 ng·h/mL, and a half-life (t1/2z) of 1.9 to 4.6 h.
*BioAv↑, Studies on the distribution of EGCG have revealed that, despite its limited absorption, it is rapidly disseminated throughout the body or quickly converted into metabolites
*BBB↑, Additionally, EGCG can cross the blood–brain barrier, allowing it to reach the brain
*hepatoP↓, Several studies have documented liver damage linked to green tea consumption [48,49,50,51,52,53].
*other↓, EGCG has also been shown to inhibit the intestinal absorption of non-heme iron in a dose-dependent manner in a controlled clinical trial
*Inflam↓, EGCG has been widely recognized for its anti-inflammatory effects
*NF-kB↓, EGCG has been shown to suppress NF-κB activation, inhibit its nuclear translocation, and block AP-1 activity
*AP-1↓,
*iNOS↓, downregulation of pro-inflammatory enzymes like iNOS and COX-2 and scavenging of ROS/RNS, including nitric oxide and peroxynitrite
*COX2↓,
*ROS↓,
*RNS↓,
*IL8↓, EGCG has been shown to suppress airway inflammation by reducing IL-8 release, a cytokine involved in neutrophil aggregation and ROS production.
*JAK↓, EGCG blocks the JAK1/2 signaling pathway
*PDGFR-BB↓, downregulate PDGFR and IGF-1R gene expression
*IGF-1R↓,
*MMP2↓, reduce MMP-2 mRNA expression
*P53↓, downregulation of the p53-p21 signaling pathway and the enhanced expression of Nrf2
*NRF2↑,
*TNF-α↓, 25 to 100 μM reduced the levels of TNF-α, IL-6, and ROS while enhancing the expression of E2F2 and superoxide dismutases (SOD1 and SOD2), enzymes vital for cellular antioxidant defense.
*IL6↓,
*E2Fs↑,
*SOD1↑,
*SOD2↑,
Casp3↑, EGCG has been shown to activate key apoptotic pathways, such as caspase-3 activation, cytochrome c release, and PARP cleavage, in various cell models, including PC12 cells exposed to oxidative stress
Cyt‑c↑,
PARP↑,
DNMTs↓, (1) the inhibition of DNA hypermethylation by blocking DNA methyltransferase (DNMT)
Telomerase↓, (2) the repression of telomerase activity;
Hif1a↓, (3) the suppression of angiogenesis via the inhibition of HIF-1α and NF-κB;
MMPs↓, (4) the prevention of cellular metastasis by inhibiting matrix metalloproteinases (MMPs);
BAX↑, (5) the promotion of apoptosis through the activation of pro-apoptotic proteins like BAX and BAK
Bak↑,
Bcl-2↓, while downregulating anti-apoptotic proteins like BCL-2 and BCL-XL;
Bcl-xL↓,
P53↑, (6) the upregulation of tumor suppressor genes such as p53 and PTEN;
PTEN↑,
TumCP↓, (7) the inhibition of inflammation and proliferation via NF-κB suppression;
MAPK↓, (8) anti-proliferative activity through the modulation of MAPK and IGF1R pathways
HGF/c-Met↓, EGCG inhibits hepatocyte growth factor (HGF), which is involved in tumor migration and invasion
TIMP1↑, EGCG has also been shown to influence the expression of tissue inhibitors of metalloproteinases (TIMPs) and MMPs, which are involved in tumorigenesis
HDAC↓, nhibition of UVB-induced DNA hypomethylation and modulation of DNMT and histone deacetylase (HDAC) activities
MMP9↓, inhibiting MMPs such as MMP-2 and MMP-9
uPA↓, EGCG may block urokinase-like plasminogen activator (uPA), a protease involved in cancer progression
GlutMet↓, EGCG can exert antitumor effects by inhibiting glycolytic enzymes, reducing glucose metabolism, and further suppressing cancer-cell growth
ChemoSen↑, EGCG’s combination with standard chemotherapy drugs may enhance their efficacy through additive or synergistic effects, while also mitigating chemotherapy-related side effects
chemoP↑,

3202- EGCG,    Epigallocatechin-3-gallate enhances ER stress-induced cancer cell apoptosis by directly targeting PARP16 activity
- in-vitro, Cerv, HeLa - in-vitro, HCC, QGY-7703
PARP16↓, (EGCG) as a potential inhibitor of PARP16.
p‑PERK↓, EGCG suppressed the ER stress-induced phosphorylation of PERK and the transcription of unfolded protein response-related genes,
Apoptosis↑, leading to dramatically increase of cancer cells apoptosis
eIF2α↓, EGCG suppressed the phosphorylation of PERK and eIF2α induced by ER stress.
UPR↓, UPR-related gene was dramatically induced by BFA and TUN, and this induction was suppressed by treatment of Hela cells with EGCG, further suggesting that EGCG suppressed the UPR induced by ER stress.
ER Stress↑, EGCG can dramatically inhibit the activity of PARP16, and then suppressed the ER stress-induced PERK phosphorylation, leading to dramatical increase of the ER stress-induced apoptosis of cancer cells.
eff↑, These results indicate that EGCG can be used in combination with ER stress-induced drugs to treat the cancer cell.
GRP78/BiP↓, EGCG had previously been found to bind to the ATP-binding domain of glucose regulate protein 78 (GRP78),

3203- EGCG,    (-)- Epigallocatechin-3-gallate induces GRP78 accumulation in the ER and shifts mesothelioma constitutive UPR into proapoptotic ER stress
- NA, MM, NA
ROS↑, We have previously shown that (-)-epigallocatechin-3-gallate (EGCG) enhances ROS production and alters Ca2+ homeostasis in cell lines deriving from therapy-recalcitrant malignant mesothelioma (MMe).
Ca+2↝,
GRP78/BiP↑, Exposure to EGCG further increased GRP78 in the ER, and induced ATF4, spliced XBP1, CHOP, and EDEM expressions, combined with a reduction of cell surface GRP78 and a rise in caspase 3 and 8 activities.
ATF4↑,
XBP-1↑,
CHOP↑,
Casp3↑,
Casp8↑,
*GRP78/BiP↓, n non-cancer mouse retinal pigment epithelial cells,EGCG has been found to downregulate GRP78 and UPR signaling (Karthikeyan et al., 2017).
*UPR↓,
UPR↑, However, if ER homeostasiscannot be re-established, the UPR switches its signaling toward irreversible ER stress with the activation of apoptosis (

3204- EGCG,    The Role of ER Stress and the Unfolded Protein Response in Cancer
- Review, Var, NA
BID↓, EGCG, a green tea polyphenol, induces ER stress-mediated apoptosis in colorectal cancer cells, an effect associated with BiP upregulation
UPR↑, Natural compounds have also been identified as BiP modulators, including palmatine and epigallocatechin gallate (EGCG), which impair BiP function, leading to unfolded protein accumulation and UPR activation.
ER Stress↑,

3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,

3206- EGCG,    Insights on the involvement of (-)-epigallocatechin gallate in ER stress-mediated apoptosis in age-related macular degeneration
- Review, AMD, NA
*Ca+2↓, EGCG restores [Ca2+]i homeostasis by decreasing ROS production through inhibition of prohibitin1 which regulate ER-mitochondrial tether site and inhibit apoptosis.
*ROS↓,
*Apoptosis↓,
*GRP78/BiP↓, EGCG downregulated GRP78, CHOP, PERK, ERO1α, IRE1α, cleaved PARP, cleaved caspase 3, caspase 12 and upregulated expression of calnexinin MRPE cells
*CHOP↓,
*PERK↓,
*IRE1↓,
*p‑PARP↓,
*Casp3↓,
*Casp12↓,
*ER Stress↓,
*UPR↓, EGCG mitigates ER stress; maintain calcium homeostasis and inhibition of UPR to control the progression of AMD.

3207- EGCG,    EGCG Enhances the Chemosensitivity of Colorectal Cancer to Irinotecan through GRP78-MediatedEndoplasmic Reticulum Stress
- in-vitro, CRC, RKO - in-vitro, CRC, HCT116
GRP78/BiP↑, Findings showed that EGCG alone or in combination with irinotecan can significantly promote intracellular GRP78 protein expression, reduce mitochondrial membrane potential and intracellular ROS in RKO and HCT 116 cells
MMP↓,
ER Stress↑, activate ERS of colorectal cancer cells,
ROS↓, EGCG Alone and in Combination with Irinotecan Inhibit ROS Production in CRC
UPR↑, EGCG can promote the transformation of constitutive UPR of colorectal cancer cells into endoplasmic reticulum stress by increasing the accumulation of intracellular GRP78 and inhibiting its cell membrane translocation.

3208- EGCG,    Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1α
- in-vitro, Colon, HT29 - in-vitro, Nor, 3T3
TumCD↓, EGCG treatment was toxic to the HT-29 cell line
ER Stress↑, EGCG induced ER stress in HT-29 by upregulating immunoglobulin-binding (BiP), PKR-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor 2 alpha subunit (eIF2α), activating transcription 4 (ATF4), and IRE1α
GRP78/BiP↑,
PERK↑,
eIF2α↑,
ATF4↑,
IRE1↑,
Apoptosis↑, Apoptosis was induced in HT-29 cells after the EGCG treatment, as shown by the Caspase 3/7 activity.
Casp3↑,
Casp7↑,
Wnt↓, (CRC) via suppression of the Wnt/β-catenin pathway
β-catenin/ZEB1↓,
*toxicity∅, This embryonic fibroblast cell line (3T3) has shown that the EGCG was not toxic to normal healthy cells, given the treatment at any concentration even at the highest concentration of EGCG (1000 μM).
UPR↑, ER stress is induced by EGCG and activates UPR proteins

3209- EGCG,    Epigallocatechin gallate upregulates NRF2 to prevent diabetic nephropathy via disabling KEAP1
- in-vitro, Diabetic, NA
*NRF2↑, EGCG is known as a potent activator of nuclear factor erythroid 2-related factor 2 (NRF2),

3210- EGCG,    Protective effect of epigallocatechin-3-gallate (EGCG) via Nrf2 pathway against oxalate-induced epithelial mesenchymal transition (EMT) of renal tubular cells
- in-vitro, Nor, NA
*ROS↓, reduced production of intracellular ROS through activation of Nrf2 signaling and increased catalase anti-oxidant enzyme.
*NRF2↑,
*Catalase↑,
*antiOx↑,

3211- EGCG,    Antioxidation Function of EGCG by Activating Nrf2/HO-1 Pathway in Mice with Coronary Heart Disease
- in-vivo, NA, NA
*cardioP↑, EGCG significantly attenuated myocardial injuries and improved blood lipid levels in mice in a concentration-dependent manner.
*VEGF↓, EGCG significantly decreased the expression of VEGFA and MMP-2 and increased the activity of superoxide dismutase (SOD), when reducing the content of reactive oxygen species (ROS) in the myocardial tissue
*MMP2↓,
*SOD↑,
*ROS↓,
*HO-1↑, and upregulating the expression of HO-1, NQO1, and Nrf2.
*NQO1↑,
*NRF2↑,

1975- EGCG,    Molecular bases of thioredoxin and thioredoxin reductase-mediated prooxidant actions of (-)-epigallocatechin-3-gallate
- in-vitro, Cerv, HeLa
TrxR↓, EGCG-induced inactivation of TrxR and decreased cell survival, revealing TrxR as a new target of EGCG.
Trx↓,
ROS↑, EGCG induced inactivation of Trx/TrxR in parallel with increased ROS levels in HeLa cells.
Dose↑, Statistics indicated that ROS levels were significantly higher within a range of 50-200uM EGCG than that at 25 uM EGCG, but there were no significant differences in ROS levels between 50 uM vs 100 uM,

1071- EGCG,    Green tea polyphenols modulate insulin secretion by inhibiting glutamate dehydrogenase
- in-vitro, Nor, NA
*GDH↓,

1072- EGCG,    Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways
- in-vitro, Thyroid, 8505C
EMT↓,
TumCI↓,
TumCMig↓,
TGF-β↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,

1303- EGCG,    (-)-Epigallocatechin-3-gallate induces apoptosis in human endometrial adenocarcinoma cells via ROS generation and p38 MAP kinase activation
- in-vitro, EC, NA
TumCP↓,
ER-α36↓,
cycD1/CCND1↓,
ERK↑,
Jun↓,
BAX↑,
Bcl-2↓,
cl‑Casp3↑,
ROS↑,
p38↑,

1503- EGCG,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
selectivity↑, EGCG has been shown to induce apoptosis and cell cycle arrest in many cancer cells without affecting normal cells
DNMT1↓, inhibition of DNMT1 leading to demethylation and reactivation of methylation-silenced genes.
RECK↑, EGCG-induced epigenetic reactivation of RECK
MMPs↓, negatively regulates matrix metalloproteinases (MMPs)
TumCI↓, inhibits tumor invasion, angiogenesis, and metastasis
angioG↓,
TumMeta↓,
HATs↓, EGCG has strong HAT inhibitory activity
IκB↑, increases the level of cytosolic IκBα
NF-kB↓, suppresses tumor necrosis factor α-induced NF-κB activation
IL6↓,
COX2↓,
NOS2↓,
ac‑H3↑, increased the levels of acetylated histone H3 (LysH9/18) and H4 levels
ac‑H4↑,
eff↑, EGCG may synergize with the HDAC inhibitory action of vorinostat to help de-repress silenced tumor suppressor genes regulating key functions such as proliferation and cell survival

1514- EGCG,    Preferential inhibition by (-)-epigallocatechin-3-gallate of the cell surface NADH oxidase and growth of transformed cells in culture
- in-vitro, Cerv, HeLa - in-vitro, Nor, MCF10
selectivity↑, EGCg preferentially inhibited growth of HeLa and mammary adenocarcinoma cells compared with growth of mammary epithelial cells
*toxicity∅, Mammary epithelial cells recovered from EGCg treatment even at 50 mM
TumCG↓, growth of HeLa and mammary adenocarcinoma cells was inhibited by EGCg at concentrations as low as 1 mM. With repeated additions of 100 nM EGCg (every 2 hr during the day), growth was inhibited during the day but recovered during the night
NADHdeh?,
eff↑, Green tea infusions were approximately 10 times more effective than those of black tea and contained approximately 10 times more EGCg
ENOX2↓, EGCg inhibit the NADH oxidase(ENOX2) of plasma membrane vesicles from cancer cells and not that of normal cells,
Dose?, with repeated additions (twice daily) at 1 mM EGCg, the EGCg concentration achieving complete inhibition of tNOX in BT-20 cells, growth inhibition and apoptosis in BT-20 cells were achieved.

1515- EGCG,  Phen,    Reciprocal Relationship Between Cytosolic NADH and ENOX2 Inhibition Triggers Sphingolipid-Induced Apoptosis in HeLa Cells
- in-vitro, Cerv, HeLa - in-vitro, Nor, MCF10 - in-vitro, BC, BT20
selectivity↑, ENOX2 INHIBITORS SLOW THE GROWTH OF HeLa CELLS AND INDUCE APOPTOSIS IN CANCER BUT NOT IN NON-CANCER CELLS
ENOX2↓,
NADH↑, INCREASED NADH RESULTING FROM ENOX2 CELL SURFACE INHIBITION INHIBITS PLASMA MEMBRANE-ASSOCIATED SPHINGOSINE KINASE (SK) AND LOWERS LEVELS OF PRO-SURVIVAL SPHINGOSINE-1-PHOSPHATE (S1P
SK↓, SK activity was decreased in response to 1.5 mM NADH
eff↑, Capsaicin added to block NADH oxidation by endo- genous ENOX2 was without effect when added alone but enhanced inhibition slightly when combined with 1.5 mM NADH
aSmase↑, SMase activity was stimulated by NADH

1516- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*Dose∅, A pharmacokinetic study in healthy individuals receiving single doses of EGCGrevealed that plasma concentrations exceeded 1 μM only with doses of >1 g
Half-Life∅, peak levels observed between 1.3 and 2.2 h (and a half-life (t1/2z) of 1.9 to 4.6 h)
BioAv∅, oral bioavailability of 20.3% relative to intravenous admistration
BBB↑, EGCG can cross the blood–brain barrier, allowing it to reach the brain
toxicity∅, Isbrucher et al. found no evidence of genotoxicity in rats following oral administration of EGCG at doses of 500, 1000, or 2000 mg/kg, or intravenous injections of 10, 25, or 50 mg/kg/day.
eff↓, interaction with the folate transporter has been reported, leading to reduced bioavailability of folic acid
Apoptosis↑,
Casp3↑,
Cyt‑c↑, cytochrome c release
cl‑PARP↑,
DNMTs↓,
Telomerase↓,
angioG↓,
Hif1a↓,
NF-kB↓,
MMPs↓,
BAX↑,
Bak↑,
Bcl-2↓,
Bcl-xL↓,
P53↑,
PTEN↑,
IGF-1↓,
H3↓,
HDAC1↓,
*LDH↓, reduces LDL cholesterol, decreases oxidative stress by neutralizing ROS
*ROS↓,

1974- EGCG,    Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes
- in-vitro, Nor, NA
*ROS↓, suppressed the increase in intracellular reactive oxygen species (ROS), nitric oxide (NO),
*NO↓,
*MMP↑, preincubation of the cells with EGCG increased mitochondrial membrane potential (MMP) and reduced calcium ion ([Ca2+]i) load.
*i-Ca+2↓, EGCC Increased Mitochondrial Membrane Potential and Decreased [Ca2+]i
*HO-1↑, expression of SOD, Heme oxygenase-1 (HO-1), Catalase (CAT), GSH-PX, nuclear factor erythroid 2-related factor 2 (Nrf2), and thioredoxin-1 (Trx-1).
*Catalase↑,
*NRF2↑,
*Trx1↑,
*antiOx↑, EGCC Increased Antioxidant Capacity
*SOD↑, EGCC Decreased ROS and Increased SOD Generation
*Apoptosis↓,

2468- EGCG,    Green tea epigallocatechin-3-gallate inhibits platelet signalling pathways triggered by both proteolytic and non-proteolytic agonists
- in-vitro, Nor, NA
*AntiAg↑, EGCG inhibits platelet activation, by hindering the thrombin proteolytic activity, and by reducing the agonist-induced [Ca(2+)](c) increase through inhibition of Syk and Lyn activities.
*Ca+2↓,

1976- EGCG,    Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cells
- in-vitro, GBM, U87MG
ROS↑, Polyphenol epigallocatechin-3-gallate (EGCG) induced apoptosis in glioma cells by elevating oxidative stress through increased reactive oxygen species (ROS) generation. Signs of apoptosis included altered mitochondrial membrane potential and elevated
MMP↓, altered mitochondrial membrane potential
Casp3↑, elevated expression of caspase-3 (5fold) and cytochrome c
Cyt‑c↑,
Trx1↓, The increase in ROS was concomitant with the decrease in expression of thioredoxin (TRX-1)
Ceru↓, and ceruloplasmin (CP)
IL6↓, EGCG downregulated the levels of pro-inflammatory cytokine interleukin (IL)-6 and chemokines IL-8, monocyte-chemoattractant protein (MCP)-1 and RANTES
IL8↓,
MCP1↓,
RANTES?,
uPA↝, 40-50% decrease in uPa activity was observed in glioma cells upon treatment with 50 and 100 uM of EGCG
ROS↑, ROS production, a significant 1.7- and 2-fold (p<0.05) increase in ROS production was observed in cells treated with 50 and 100 uM EGCG respectively,

2302- EGCG,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
TumCP↓, EGCG suppressed proliferation and dose-dependently inhibited the expression of HIF-1α
Hif1a↓, EGCG significantly suppressed HIF-1α protein accumulation in these cells but did not affect HIF-1α mRNA expression.
LDHA↓, Moreover, EGCG attenuated LDHA release in Sarcoma 180 tumor-bearing mice
PFK↓, Moreover, EGCG inhibited the expression and activity of PFK in hepatocellular carcinoma (HCC-LM3 and HepG2) cells
cardioP↑, EGCG-exerted heart benefits related to reduced LDH release
Glycolysis↓, EGCG inhibits glycolysis (especially PFK activity) in aerobic glycolytic HCC cell lines
PKM2↓, EGCG inhibits glycolysis through repressing rate-limiting enzymes (PFK and PKM2)

2309- EGCG,  Chemo,    Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HPNE - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumCG↓, EGCG reduced pancreatic cancer cell growth in a concentration-dependent manner
eff↑, and the growth inhibition effect was further enhanced under glucose deprivation conditions.
ROS↑, EGCG at 40 µM increased ROS levels by 1.4- and 1.6-fold in Panc-1 and MIA PaCa-2 cells, respectively
ECAR↓, EGCG affected glycolysis by suppressing the extracellular acidification rate through the reduction of the activity and levels of the glycolytic enzymes phosphofructokinase and pyruvate kinase.
ChemoSen↑, EGCG sensitized gemcitabine to inhibit pancreatic cancer cell growth in vitro and in vivo.
selectivity↑, EGCG at 80 µM for 72 h had significantly less effect on the HPNE cells, reducing cell growth by only 24%
Glycolysis↓, EGCG Inhibits Glycolysis through Suppressing Rate-Limiting Enzymes. EGCG Plus Gemcitabine Further Inhibits Glycolysis
PFK↓, EGCG treatment reduced both the activity and expression levels of phosphofructokinase (PFK) and pyruvate kinase (PK) in Panc-1 and MIA PaCa-2 cells
PKA↓,
HK2∅, EGCG failed to reduce hexokinases II (HK2) and lactate dehydrogenase A (LDHA) protein expression levels
LDHA∅,
PFKP↓, EGCG reduced the levels of PFKP and PKM2 (p < 0.01 for both) in pancreatic tumor xenograft homogenates, obtained from mice treated with EGCG
PKM2↓,
H2O2↑, EGCG at 40 µM increased H2O2 levels by 1.5- and 1.9-fold in Panc-1 and MIA PaCa-2 cells
TumW↓, EGCG and gemcitabine, given as single agents, reduced tumor weight by 40% and 52%, respectively, compared to vehicle-treated controls (p < 0.05 and p < 0.01). In combination, EGCG plus gemcitabine reduced tumor weight by 67%,

2310- EGCG,    Epigallocatechin-3-gallate downregulates PDHA1 interfering the metabolic pathways in human herpesvirus 8 harboring primary effusion lymphoma cells
- in-vitro, lymphoma, PEL
GLUT3↑, EGCG increased GLUT3 and decreased PDHA1 and GDH1 expression to disrupt glycolysis and glutaminolysis in PEL cells
PDHA1↓,
GDH↓,
ROS↑, Previously we have demonstrated that EGCG induces ROS generation and cell death in HHV8 harboring PEL cells
Glycolysis↓, EGCG induced PEL cell death may due to suppresses both the aerobic glycolysis and oxidative phosphorylation
OXPHOS↓,

2395- EGCG,    EGCG inhibits diabetic nephrophathy through up regulation of PKM2
- Study, Diabetic, NA
*PKM2↑, pigallocatechin (EGCG), isolated from Green tea, increases Pyruvate kinase M2 (PKM2) expression, decreases toxic glucose metabolites, mitochondrial dysfunction and apoptosis, augments glycolytic flux and PGC-1α levels
*Apoptosis↓,
*PGC-1α↑,

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

3213- EGCG,  Rad,    Epigallocatechin-3-gallate Enhances Radiation Sensitivity in Colorectal Cancer Cells Through Nrf2 Activation and Autophagy
- in-vitro, CRC, HCT116
RadioS↑, Combination treatment with EGCG and radiation significantly decreased the growth of HCT-116 cells.
TumCP↓, EGCG increased the sensitivity of colorectal cancer cells to radiation by inhibiting cell proliferation and inducing Nrf2 nuclear translocation and autophagy.
NRF2↑,

2460- EGCG,  Taur,    Anti-fibrosis activity of combination therapy with epigallocatechin gallate, taurine and genistein by regulating glycolysis, gluconeogenesis, and ribosomal and lysosomal signaling pathways in HSC-T6 cells
- in-vitro, Nor, HSC-T6
HK2↓, The results of the present study indicate that combination treatment with taurine, EGCG and genistein significantly inhibits the expression of HK2.

3240- EGCG,    Green tea constituents (−)-epigallocatechin-3-gallate (EGCG) and gallic acid induce topoisomerase I– and topoisomerase II–DNA complexes in cells mediated by pyrogallol-induced hydrogen peroxide
- in-vitro, AML, K562
TOP1↑, induce topoisomerase I– and topoisomerase II–DNA complexes in cells mediated by pyrogallol-induced hydrogen peroxide
TOP2↑,

3231- EGCG,    Epigallocatechin-3-gallate restores mitochondrial homeostasis impairment by inhibiting HDAC1-mediated NRF1 histone deacetylation in cardiac hypertrophy
- in-vitro, Nor, NA
*HDAC↓, Administration of epigallocatechin-3-gallate (EGCG), an inhibitor of HDAC1, restored cardiac function, decreased heart/body weight and fibrosis
*cardioP↑,
*Nrf1↑, EGCG upregulated both NRF1 and PGC-1α in vitro
*PGC-1α↓,


Showing Research Papers: 1 to 50 of 180
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 180

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ceru↓, 1,   ENOX2↓, 2,   H2O2↑, 1,   NADH↑, 1,   NADHdeh?, 1,   NRF2↑, 1,   OXPHOS↓, 1,   ROS↓, 1,   ROS↑, 10,   Trx↓, 1,   Trx1↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   GDH↓, 1,   GlucoseCon↓, 1,   GlutMet↓, 1,   Glycolysis↓, 4,   HK2↓, 4,   HK2∅, 1,   lactateProd↓, 2,   LDHA↓, 1,   LDHA∅, 1,   PDHA1↓, 1,   PFK↓, 2,   PFKP↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 4,   aSmase↑, 1,   BAD↑, 1,   Bak↑, 3,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 2,   BID↓, 1,   Casp↑, 1,   Casp3↑, 6,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↓, 1,   Casp8↑, 2,   Cyt‑c↑, 3,   Fas↑, 1,   HGF/c-Met↓, 1,   MAPK↓, 1,   Myc↓, 1,   p38↑, 1,   SK↓, 1,   Telomerase↓, 2,   TumCD↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 2,   Sp1/3/4↑, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   ac‑H3↑, 1,   ac‑H4↑, 1,   HATs↓, 1,   other↝, 1,   other∅, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   eIF2α↓, 1,   eIF2α↑, 1,   ER Stress↑, 5,   GRP78/BiP↓, 1,   GRP78/BiP↑, 4,   HSP27↓, 1,   IRE1↑, 1,   PERK↑, 1,   p‑PERK↓, 1,   UPR↓, 1,   UPR↑, 5,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMTs↓, 2,   P53↑, 2,   PARP↑, 2,   cl‑PARP↑, 1,   TP53↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 2,   EMT↓, 1,   ERK↓, 2,   ERK↑, 1,   HDAC↓, 1,   HDAC1↓, 1,   IGF-1↓, 1,   IGF-1R↑, 1,   Jun↓, 1,   NOTCH3↓, 1,   PTEN↑, 2,   STAT3↓, 1,   p‑STAT3↓, 1,   TOP1↑, 1,   TOP2↑, 1,   TumCG↓, 3,   Wnt↓, 1,   Wnt↑, 1,  

Migration ⓘ

AntiAg↑, 3,   AP-1↓, 1,   Ca+2↝, 1,   ER-α36↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMP9↑, 1,   MMPs↓, 4,   p‑PDGF↓, 1,   PKA↓, 1,   RECK↑, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   SMAD4↓, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 6,   TumMeta↓, 1,   uPA↓, 1,   uPA↝, 1,   Zeb1↑, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 3,   EGFR↓, 1,   Hif1a↓, 3,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT3↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   IκB↑, 1,   MCP1↓, 1,   NF-kB↓, 6,   PSA↓, 1,   RANTES?, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv∅, 1,   ChemoSen↑, 2,   Dose?, 1,   Dose↑, 1,   Dose↝, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 9,   Half-Life↝, 1,   Half-Life∅, 1,   RadioS↑, 1,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   IL6↓, 2,   Myc↓, 1,   NOS2↓, 1,   PSA↓, 1,   TP53↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   chemoP↑, 2,   chemoPv↑, 1,   OS↑, 2,   PARP16↓, 1,   Remission↓, 1,   Remission↑, 1,   toxicity∅, 1,   TumW↓, 1,  
Total Targets: 181

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 2,   HO-1↑, 2,   MPO↓, 1,   NQO1↑, 1,   Nrf1↑, 1,   NRF2↑, 6,   RNS↓, 1,   ROS↓, 8,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,   Trx1↑, 1,  

Mitochondria & Bioenergetics ⓘ

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

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↓, 1,   AMPK↑, 1,   CRM↓, 1,   GDH↓, 1,   glucose↓, 1,   LDH↓, 1,   LDL↓, 2,   PKM2↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 3,   BAX↓, 1,   Casp12↓, 1,   Casp3↓, 1,   Cyt‑c↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 2,   IRE1↓, 1,   PERK↓, 1,   UPR↓, 2,  

DNA Damage & Repair ⓘ

P53↓, 1,   p‑PARP↓, 1,  

Cell Cycle & Senescence ⓘ

E2Fs↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   IGF-1R↓, 1,   mTORC1↓, 1,  

Migration ⓘ

AntiAg↑, 1,   AP-1↓, 1,   Ca+2?, 1,   Ca+2↓, 2,   i-Ca+2↓, 1,   MMP2↓, 2,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   PDGFR-BB↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 2,   JAK↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   Dose?, 1,   Dose↝, 1,   Dose∅, 1,   eff↑, 2,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   cardioP↑, 4,   hepatoP↓, 1,   memory↑, 1,   neuroP↑, 2,   OS↑, 1,   RenoP↑, 1,   toxicity∅, 2,  
Total Targets: 84

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=on  sortOrder:rid,rpid

 

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