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">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


Scientific Papers found: Click to Expand⟱
147- AG,  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↑,
NF-kB↓,
PI3K/Akt↓,
STAT3↓,

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.

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

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↑, protein expression

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↑,

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↓,
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,  Tau,    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.

3239- EGCG,    (−)-Epigallocatechin Gallate, A Major Constituent of Green Tea, Poisons Human Type II Topoisomerases
*TOP2↑, Enhancement of Topoisomerase II-mediated DNA Cleavage by Green Tea Extract

3230- EGCG,    Green Tea Polyphenol Epigallocatechin 3-Gallate, Contributes to the Degradation of DNMT3A and HDAC3 in HCT 116 Human Colon Cancer Cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29
HDAC↓, HDAC and DNMT protein expression was reduced when methylation-sensitive HCT 116 human colon cancer cells was treated with EGCG, but was relatively stable in the HT-29 cell line.
DNMTs↓,

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↓,

3232- EGCG,    (−)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer׳s disease model mice by upregulating neprilysin expression
- in-vivo, AD, NA
HDAC1↓, EGCG down-regulated APP expression both in Alzheimer׳s disease (AD) and tumor, which associated with HDAC1 inhibition in tumor.
*HDAC1↓,
*Aβ↓, EGCG reduced neurotoxic β-amyloid (Aβ) accumulation and rescued cognitive deterioration in AD mice model.
*cognitive↑,

3233- EGCG,    Epigallocatechin gallate inhibits HeLa cells by modulation of epigenetics and signaling pathways
- in-vitro, Cerv, HeLa
DNMTs↓, EGCG may competitively inhibit some epigenetic enzymes (DNMT1, DNMT3A, HDAC2, HDAC3, HDAC4, HDAC7 and EZH2).
DNMT1↓,
DNMT3A↓,
HDAC2↓,
HDAC3↓,
HDAC4↓,
EZH2↓, Interaction of EGCG with EZH2 protein indicates inhibition of activity
PI3K↓, Downregulation of key signaling moieties of PI3K, Wnt and MAPK pathways
Wnt↓,
MAPK↓,
hTERT↓, including TERT, CCNB1, CCNB2, MMP2, MMP7. PIK3C2B, PIK3CA, MAPK8 and IL6 was also observed
MMP2↓,
MMP7↓,
IL6↓,
MDM2↓, Fig 1
MMP-10↓,
TP53↑,
PTEN↑,

3234- EGCG,  Rad,    EGCG, a tea polyphenol, as a potential mitigator of hematopoietic radiation injury in mice
- in-vivo, Nor, NA
*DNMTs↓, EGCG (epigallocatechin gallate), a tea polyphenol with known DNMT inhibitory property, in C57 Bl/6 mice model.
*radioP↑, EGCG reduced cytogenetic damage to bone marrow cells in radiation exposed mice significantly
*HDAC↑, ELISA assay with bone marrow cell lysates showed EGCG as an inhibitor of HDAC activity

3235- EGCG,    (-)-Epigallocatechin-3-gallate reverses the expression of various tumor-suppressor genes by inhibiting DNA methyltransferases and histone deacetylases in human cervical cancer cells
- in-vivo, Cerv, HeLa
DNMTs↓, In the present study, time-dependent EGCG-treated HeLa cells were found to have a significant reduction in the enzymatic activity of DNMT and HDAC
HDAC↓,

3236- EGCG,  BA,    Molecular mechanisms for inhibition of colon cancer cells by combined epigenetic-modulating epigallocatechin gallate and sodium butyrate
- in-vitro, Colon, RKO - in-vitro, Colon, HCT116 - in-vitro, Colon, HT29
Apoptosis↑, combination treatment induced apoptosis and cell cycle arrest in RKO, HCT-116 and HT-29 colorectal cancer cells.
TumCCA?,
HDAC1↓, decrease in HDAC1, DNMT1, survivin and HDAC activity in all three cell lines.
DNMT1↓,
survivin↓,
HDAC↓,
P21↑, induction of p21 and an increase in nuclear factor kappa B (NF-κB)-p65.
NF-kB↑,
γH2AX↑, An increase in double strand breaks as determined by gamma-H2A histone family member X (γ-H2AX) protein levels
ac‑H3↑, induction of histone H3 hyperacetylation was also observed with combination treatment.
DNAdam↑,

3237- EGCG,    (-)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer's disease model mice by upregulating neprilysin expression
- in-vivo, AD, NA
*HDAC↓, We previously reported that (-)-epigallocatechin-3-gallate (EGCG) acts as an HDAC inhibitor
*Aβ↓, Here, we demonstrate that EGCG reduced β-amyloid (Aβ) accumulation in vitro and rescued cognitive deterioration in senescence-accelerated mice
cognitive↑,

3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, EGCG stimulates telomere fragmentation through inhibiting telomerase activity.
DNMTs↓, EGCG reduced DNMTs,
cycD1↓, EGCG also reduced the protein expression of cyclin D1, cyclin E, CDK2, CDK4, and CDK6. EGCG also inhibited the activity of CDK2 and CDK4, and caused Rb hypophosphorylation
cycE↓,
CDK2↓,
CDK4↓,
CDK6↓,
HATs↓, EGCG can inhibit certain biomedically important molecular targets such as DNMTs, HATs, and HDACs
HDAC↓,
selectivity↑, EGCG has shown higher cytotoxicity in cancer cells than in their normal counterparts.
uPA↓, EGCG blocks urokinase, an enzyme which is essential for cancer growth and metastasis
NF-kB↓, EGCG inhibits NFκB and expression of TNF-α, reduces cancer promotion
TNF-α↓,
*ROS↓, It acts as strong ROS scavenger and antioxidant,
*antiOx↑,
Hif1a↓, ↓ HIF-1α; ↓ VEGF; ↓ VEGFR1;
VEGF↓,
MMP2↓, ↓ MMP-2; ↓ MMP-9; ↓ FAK;
MMP9↓,
FAK↓,
TIMP2↑, TIMP-2; ↑
Mcl-1↓, ↓ Mcl-1; ↓ survivin; ↓ XIAP
survivin↓,
XIAP↓,
PCNA↓, ↓ PCNA; ↑ 16; ↑ p18; ↑ p21; ↑ p27; ↑ pRb; ↑ p53; ↑ mdm2
p16↑,
P21↑,
p27↑,
pRB↑,
P53↑,
MDM2↑,
ROS↑, ↑ ROS; ↑ caspase-3; ↑ caspase-8; ↑ caspase-9; ↑ cytochrome c; ↑ Smac/DIABLO; ↓↑ Bax; Z Bak; ↓ cleaved PPAR;
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑,
Diablo↑,
BAX⇅,
cl‑PPARα↓,
PDGF↓, ↓ PDGF; ↓ PDGFRb; ↓ EGFR;
EGFR↓,
FOXO↑, activated FOXO transcription factors
AP-1↓, The inhibition of AP-1 activity by EGCG was associated with inhibition of JNK activation but not ERK activation.
JNK↓,
COX2↓, EGCG reduces the activity of COX-2 following interleukin-1A stimulation of human chondrocytes
angioG↓, EGCG inhibits angiogenesis by enhancing FOXO transcriptional activity

3229- EGCG,    Epigallocatechin-3-gallate (EGCG) Alters Histone Acetylation and Methylation and Impacts Chromatin Architecture Profile in Human Endothelial Cells
- in-vitro, Nor, HMEC - in-vitro, Nor, HUVECs
HDAC↓, We also found that the catechin acts as an HDAC inhibitor in cellular and cell-free models

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↑,

3241- EGCG,    Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
tumCV↓, EGCG treatment decreased cell viability and increased mitochondrial damage‐triggered apoptosis in both HCT116 and HT‐29 cancer cells
mtDam↑,
Apoptosis↑,
ATP↓, Suppression of ATP synthesis by EGCG
lipoGen↓, depletion of lipogenesis in the DNL pathway,
eff↑, Antiproliferative activity of EGCG and 5FU reduces tumor progression in a nude mouse xenograft model

3242- EGCG,    Epigallocatechin gallate has pleiotropic effects on transmembrane signaling by altering the embedding of transmembrane domains
ITGB3↓, We report that EGCG inhibits talin-induced integrin αIIbβ3 activation, but it activates αIIbβ3 in the absence of talin both in a purified system and in cells

3243- EGCG,    (−)-Epigallocatechin-3-Gallate Inhibits Colorectal Cancer Stem Cells by Suppressing Wnt/β-Catenin Pathway
CD133↓, used to determine the expression of CD133. We revealed that EGCG inhibited the spheroid formation capability of colorectal cancer cells as well as the expression of colorectal CSC markers, along with suppression of cell proliferation and induction o
CSCs↓,
TumCP↓,
Apoptosis↑,
Wnt↓, EGCG downregulated the activation of Wnt/β-catenin pathway,
β-catenin/ZEB1↓,

3244- EGCG,    Novel epigallocatechin gallate (EGCG) analogs activate AMP-activated protein kinase pathway and target cancer stem cells
AMPK↑, In this study we demonstrated that synthetic EGCG analogs 4 and 6 were more potent AMPK activators than metformin and EGCG.
TumCP↓, EGCG analogs resulted in inhibition of cell proliferation, up-regulation of the cyclin-dependent kinase inhibitor p21, down-regulation of mTOR pathway, and suppression of stem cell population in human breast cancer cells.
P21↑,
mTOR↓,
CSCs↓,
CD44↓, Both EGCG analogs 4 and 6 significantly decreased the CD44+high/CD24-low population in breast cancer cells
CD24↓,

3245- EGCG,    (−)-Epigallocatechin-3-gallate protects PC12 cells against corticosterone-induced neurotoxicity via the hedgehog signaling pathway
- in-vitro, Nor, PC12
*neuroP↑, EGCG-mediated neuroprotective effects, as well as upregulation of the Shh pathway
*Shh↑,
*Gli1↑, reversed the decrease in the levels of Shh, Gli1 and N-myc mRNA (P<0.05; Fig. 3B) and expression of N-myc protein (P<0.05; Fig. 3C) induced by 400 µM CORT.
*n-MYC↑,
*Dose↝, Higher doses of EGCG exhibit pro-oxidant and pro-apoptotic effects, whereas lower doses of EGCG have neuroprotective effects

3246- EGCG,    Epigallocatechin gallate suppresses hepatic cholesterol synthesis by targeting SREBP-2 through SIRT1/FOXO1 signaling pathway
- in-vitro, Nor, NA
*MDA↓, EGCG remarkably diminished MDA content in the liver with hypercholesterolemia and increased T-AOC and SOD activity.
*SOD↑,
*SIRT1↑, EGCG activated SIRT1 and increased FOXO1 expression
*FOXO1↑,
*SREBP2↓, EGCG increased FOXO1 expression, and decrease SREBP-2 expression

3428- EGCG,    Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein Complex
- Review, Var, NA
TumCCA↑, Our previous work revealed that epigallocatechin-3-gallate (EGCG) induced cell cycle arrest and apoptosis in Jurkat cells by the downregulation of UHRF1 and DNMT1, and the upregulation of the tumor suppressor p16
UHRF1↓,
DNMT1↓,
p16↑,

3220- EGCG,    Dual Roles of Nrf2 in Cancer
- in-vitro, Lung, A549
NRF2↑, Examples of potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany
eff↓, A549 is more resistant to cisplatin and EGCG induced cell death than any other lung cancer cell line. This was contributed to the high expression of Nrf2 and HMOX-1

3212- EGCG,    EGCG maintained Nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cells
- in-vitro, Lung, A549 - in-vivo, Lung, NCIH23
NRF2⇅, In A549, EGCG downregulated nuclear Nrf2 by upregulating the nuclear localization of Keap1 whereas in NCIH23, EGCG augmented Nrf2 by reducing Keap1.
eff↑, Though the direction of Nrf2 regulation was opposite in two cell lines, optimum level of Nrf2 was maintained which increased responsiveness towards etoposide. EGCG sensitized/potentiated lung adenocarcinoma cells towards chemotherapy by inducing G2/
SOD1↑, n NCIH23, the downstream targets of Nrf2, NQO1 and MRP1 did not show any significant alteration in expression with respect to control, with an exception of SOD1(upregulated by 1.28 times)
SOD1↓, EGCG showed exactly opposite effect in A549. It again effectively fitted in a U-shaped hormetic downregulation for all three downstream targets. EGCG (0.5 μM/12 h) most effectively downregulated SOD-1, NQO1 and MRP1expression
MMP2⇅, However, EGCG (0.5 μM) itself increased the activity of MMP-2 and MMP-9. The lowest dose of EGCG required to inhibit MMP-2 and MMP-9 was reported, 8–13 μM in different cancer cell lines
MMP9⇅,

1036- EGCG,    Green Tea Catechin Is an Alternative Immune Checkpoint Inhibitor that Inhibits PD-L1 Expression and Lung Tumor Growth
- in-vitro, Lung, A549 - in-vitro, Lung, LU99
PD-L1↓, 50 µM EGCG decreased PD-L1 mRNA by 86% (from 5.8-fold to 0.8-fold) and PD-L1 protein by 79%
EGF↓,
Akt↓,

3214- EGCG,    EGCG-induced selective death of cancer cells through autophagy-dependent regulation of the p62-mediated antioxidant survival pathway
- in-vitro, Nor, MRC-5 - in-vitro, Cerv, HeLa - in-vitro, Nor, HEK293 - in-vitro, BC, MDA-MB-231 - in-vitro, CRC, HCT116
mTOR↓, In contrast, EGCG treatment in HeLa cells led to AMPK-induced mTOR inactivation
AMPK↑, via AMPK activation,
selectivity↑, EGCG was previously reported to differentially induce ROS production in normal and cancer cells, resulting in the preferential perturbation of the redox homeostasis of cancer cells via increased ROS levels, especially H2O2, in cancer cells
ROS↑,
selectivity↑, EGCG-induced selective death of cancer cells is accomplished by the positive and negative regulation of the p62-KEAP1-NRF2-HO-1 antioxidant survival pathway between normal cells and cancer cells, respectively,
HO-1↓, HO-1 expression decreased significantly with increasing EGCG concentration in all six different cancer cells
*NRF2↑, According to our findings, EGCG increased the protein level of NRF2 in normal cells but decreased them in cancer cells even though its mRNA levels were more or less equal in both cell types
NRF2↓,
*HO-1↑, upregulates HO-1 through the prolonged stability of NRF2 in MRC5 cells, whereas it downregulates HO-1 through the increased degradation of NRF2 by ubiquitination in HeLa and HCT116 cells.

3215- EGCG,    Epigallocatechin gallate modulates ferroptosis through downregulation of tsRNA-13502 in non-small cell lung cancer
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, EGCG resulted in a notable suppression of cell proliferation, as evidenced by a reduction in Ki67 immunofluorescence staining
Ki-67↓,
GPx4↓, EGCG treatment led to a decrease in the expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) while increasing the levels of acyl-CoA synthetase long-chain family member 4 (ACSL4).
ACSL4↑,
Iron↑, accompanied by an increase in intracellular iron, malondialdehyde (MDA), and reactive oxygen species (ROS), alongside ultrastructural alterations characteristic of ferroptosis.
MDA↑,
ROS↑,
Ferroptosis↑,
eff↑, The cooperative effect of metformin and EGCG-activated Nrf2/HO-1 signaling pathway, facilitated by SIRT1-mediated Nrf2 deacetylation, enhances the susceptibility of NSCLC to EGCG modulation by promoting reactive oxygen species (ROS) generation and a
NRF2↑,
HO-1↑,

3216- EGCG,    Epigallocatechin-3-gallate suppresses hemin-aggravated colon carcinogenesis through Nrf2-inhibited mitochondrial reactive oxygen species accumulation
- NA, Colon, Caco-2
NRF2↑, EGCG enhanced hemin-induced Nrf2 and antioxidant gene expression
TumCP↓, EGCG reduced hemin-induced proliferation and colon carcinogenesis through Nrf2-inhibited mitochondrial ROS accumulation.
mt-ROS↓,
Keap1↓, We found that hemin treatment increased Nrf2 expression, but decreased Keap1 expression in a time-dependent manner

3217- EGCG,    Epigallocatechin-3-gallate promotes angiogenesis via up-regulation of Nfr2 signaling pathway in a mouse model of ischemic stroke
- in-vivo, Stroke, NA
*angioG↑, angiogenic and neuroprotective effects of EGCG
*neuroG↑,
*NRF2↑, via upregulation of Nrf2 signaling pathway.

3218- EGCG,    Comparative efficacy of epigallocatechin-3-gallate against H2O2-induced ROS in cervical cancer biopsies and HeLa cell lines
- in-vitro, Cerv, HeLa
SOD↑, activity of SOD and GPx ameliorated significantly by 117% and 264.2%, respectively
GPx↑,
*antiOx↑, EGCG, a natural antioxidant,
ROS↓, indicating EGCG to be an effective natural antioxidant combating ROS, generated as a consequence of cellular activation in cancerous cells.

3219- EGCG,    Nano-chemotherapeutic efficacy of (−) -epigallocatechin 3-gallate mediating apoptosis in A549 cells: Involvement of reactive oxygen species mediated Nrf2/Keap1signaling
- in-vitro, Lung, A549
ROS↑, Nano EGCG exhibited increased ROS/RNS levels and decreased mitochondrial membrane potential
RNS↓,
MMP↓,
NRF2↑, EGCG exhibited an increased expression of Nrf2 and Keap1 that could regulate apoptosis in A549 cells.
Keap1↓,

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↑,

3221- EGCG,    EGCG upregulates phase-2 detoxifying and antioxidant enzymes via the Nrf2 signaling pathway in human breast epithelial cells
- in-vitro, Nor, MCF10
*antiOx↑, EGCG upregulated the expression of other antioxidant enzymes, including manganese superoxide dismutase and glutathione S-transferase π in a concentration- and time-dependent manner.
*GSTA1↑,
*NRF2↑, The nuclear accumulation and ARE/EpRE binding of Nrf2 were increased in EGCG-treated MCF10A cells

3222- EGCG,    Epigallocatechin gallate and mitochondria—A story of life and death
- Review, Nor, NA
*lipid-P↓, ↓Lipid peroxidation ↑SOD, CAT, GPx, GR, and GST, ↑GSH
*SOD↑,
*Catalase↑,
GPx↑,
*GR↑,
*GSTs↑,
*GSH↑,
*SIRT1↑, EGCG upregulated the levels of NAD+ -dependent protein deacetylase sirtuin-1 (SIRT1), peroxi- some proliferator-activated receptor  co-activator-1 (PGC-1), glutathione peroxidase (GPx), and SOD in MPP + -treated PC12 cells.
*PGC1A↑,
*other↑, EGCG (2 mg/kg day-1 administered through oral gavage for 30 days) upregulated the activities of brain mitochondrial antioxidant enzymes (SOD, CAT, and GPx) in aged, but not in young rats.

3223- EGCG,    The Effects of Green Tea Catechins in Hematological Malignancies
- Review, AML, NA
Prx↓, In IM9 multiple myeloma cells, EGCG reduced the protein levels of peroxiredoxin V (Prdx V, which catalyzes the reduction in hydrogen peroxide), inducing ROS accumulation and cell death
ROS↑,

3224- EGCG,    Epigallocatechin-3-Gallate Prevents Acute Gout by Suppressing NLRP3 Inflammasome Activation and Mitochondrial DNA Synthesis
- in-vitro, Nor, NA
*Casp1↓, EGCG blocked MSU crystal-induced production of caspase-1(p10) and interleukin-1β in primary mouse macrophages, indicating its suppressive effect on the NLRP3 inflammasome.
*NLRP3↓,
*Inflam↓, contributing to the prevention of gouty inflammation

3225- EGCG,    Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling Pathway
- in-vitro, Nor, NA - in-vivo, Nor, NA
*RenoP↑, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage.
*NLRP3↓, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including TXNIP, ASC, caspase‐1, and IL‐1β, as well as the levels of ROS and inflammatory factors such as TNF‐α, IL‐6, and IL‐18.
*TXNIP↓,
*ASC↓,
*Casp1↓,
*IL1β↓,
*ROS↓,
*TNF-α↓,
*IL6↓,
*IL18↓,

3226- EGCG,    Epigallocatechin-3-gallate, a green-tea polyphenol, suppresses Rho signaling in TWNT-4 human hepatic stellate cells
- in-vitro, Nor, NA
*Rho↓, EGCG inhibited stress-fiber formation, an indicator of Rho activation, and changed the distribution of alpha-smooth-muscle actin.
other↑, suggest that EGCG has therapeutic potential in the setting of liver fibrosis.

3227- EGCG,    Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury
- NA, Nor, NA
*Rho↓, EGCG treatment is able to reduce the expression of RhoA in the injured spinal cord
*IL1↓, EGCG treatment reduces the expression of pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-alpha) and modulates the expression of a transcription factor (NF-κB) and a small GTPase (RhoA) in the spinal cord
*IL6↓,
*TNF-α↓,

3228- EGCG,    Targeting fibrotic signaling pathways by EGCG as a therapeutic strategy for uterine fibroids
*cycD1↓, Cyclin D1, a protein involved in cell cycle progression, was increased in fibroid cells and was significantly reduced by EGCG
*COL1A1↓, EGCG treatment significantly reduced mRNA or protein levels of key fibrotic proteins, including fibronectin (FN1), collagen (COL1A1), plasminogen activator inhibitor-1 (PAI-1), connective tissue growth factor (CTGF), and actin alpha 2, smooth muscle
*ACTA2↓,
*α-SMA↓, EGCG treatment severely reduced (71%) α-SMA protein expression in P57 fibroid cells but not in P57 myometrial cells, compared to control (100%)

658- EGCG,  MNPs,  MF,    Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio Interface
- in-vitro, GBM, LN229
*BioEnh↑, (EGCG), a major tea catechin, enhances cellular uptake of magnetic nanoparticles (MNPs

649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, increase EGCG bioavailability is using other natural products such as curcumin and piperine
EGFR↓,
HER2/EBBR2↓,
IGF-1↓,
MAPK↓,
ERK↓, reduction in ERK1/2 phosphorylation
RAS↓,
Raf↓, Raf-1
NF-kB↓, Numerous investigations have proven that EGCG has an inhibitory effect on NF-κB
p‑pRB↓, EGCG were displayed to reduce the phosphorylation of Rb, and as a result, cells were arrested in G1 phase
TumCCA↑, arrested in G1 phase
Glycolysis↓, EGCG has been found to inhibit key enzymes involved in glycolysis, such as hexokinase and pyruvate kinase, thereby disrupting the Warburg effect and inhibiting tumor cell growth
Warburg↓,
HK2↓,
Pyruv↓,

650- EGCG,    Cellular thiol status-dependent inhibition of tumor cell growth via modulation of retinoblastoma protein phosphorylation by (-)-epigallocatechin
- in-vitro, NA, NA
TumCCA↑, in the G1 phase
p‑pRB↓,

651- EGCG,    Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications
ROS↑, mounting evidence that EGCG can stimulate ROS production, which in turn leads to the phosphorylation and activation of AMPK
p‑AMPK↑,
mTOR↓,
FAK↓,
Smo↓,
Gli1↓,
HH↓,
TumCMig↓,
TumCI↓,
NOTCH↓,
JAK↓,
STAT↓,
Bcl-2↓,
Bcl-xL↓,
BAX↑,
Casp9↑,

652- EGCG,  VitK2,  CUR,    Case Report of Unexpectedly Long Survival of Patient With Chronic Lymphocytic Leukemia: Why Integrative Methods Matter
- Case Report, CLL, NA
Remission↑, patient has remained asymptomatic for more than 15 years

653- EGCG,    Phase 2 Trial of Daily, Oral Polyphenon E in Patients with Asymptomatic, Rai Stage 0-II Chronic Lymphocytic Leukemia(CLL)
- Trial, CLL, NA
ALC↓, (31%) patients experiencing a sustained ≥20% reduction in ALC
Remission↑, One patient treated at the phase II dose level of the phase I trial achieved a partial remission

654- EGCG,  MNPs,  MF,    Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potential
- in-vitro, Var, NA
*BioEnh↑, (EGCG) has been known to greatly enhance MNP uptake by tumor cells

655- EGCG,    A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cells
- in-vitro, HCC, HepG2
AFP↓, EGCG can effectively reduce AFP secretion and simultaneously induce AFP aggregation in human HCC HepG2 cells.
TumAuto↑,
LC3II↑, promoting the synthesis of LC3-II, a characteristic autophagosomal marke
TumCG↓,
MMP↓,

657- EGCG,  MNPs,  MF,    Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cells
- in-vitro, GBM, U87MG
*BioEnh↑, enhances MNP internalization by 3.1-fold

648- EGCG,    Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional Strategies in Healthy Volunteers
- Human, Nor, NA
*BioAv↑, green tea extract should be ingested alone after overnight fasting to optimize the gastrointestinal absorption of the EGCG.

659- EGCG,  MNPs,  MF,    Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interaction
- in-vivo, Nor, NA
*BioEnh↑, EGCG at a concentration as low as 1-3 μM, which increased MNP uptake 2- to 7-fold. In addition, application of magnetic force further potentiated MNP uptake, suggesting a synergetic effect of EGCG and magnetic force

660- EGCG,  FA,    Epigallocatechin-3-gallate Delivered in Nanoparticles Increases Cytotoxicity in Three Breast Carcinoma Cell Lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
Apoptosis↑, EGCG nanodelivery lower concentrations
*toxicity↓, We can confirm that EGCG do not harm normal cells, either delivered in LNPs or free
*eff↓, preferentially entered cancer cells whereas they were poorly assumed by normal cells

661- EGCG,  GoldNP,    Epigallocatechin-3-Gallate-Loaded Gold Nanoparticles: Preparation and Evaluation of Anticancer Efficacy in Ehrlich Tumor-Bearing Mice
- vitro+vivo, NA, NA
Apoptosis↑, EGCG-GNPs had significantly better in vivo anticancer efficacy
TumVol↓, half size compared to control

662- EGCG,    Advanced Nanovehicles-Enabled Delivery Systems of Epigallocatechin Gallate for Cancer Therapy
- Review, Var, NA
*BioEnh↑, EGCG-loaded nanovehicles has been generally recognized to enhance the stability and bioavailability of EGCG

663- EGCG,    EGCG-coated silver nanoparticles self-assemble with selenium nanowires for treatment of drug-resistant bacterial infections by generating ROS and disrupting biofilms
- in-vitro, NA, NA
ROS↑, Bacteria

664- EGCG,  SNP,    Epigallocatechin-3-gallate-capped Ag nanoparticles: preparation and characterization
- Analysis, NA, NA
other↑, polyphenolic groups of epigallocatechin-3-gallate (EGCG) are responsible for the rapid reduction of Ag+ ions into metallic Ag0

1056- EGCG,    EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression
- vitro+vivo, BC, E0771
TumW↓,
VEGF↓,
Weight∅, no effects on the body weight, heart weight, angiogenesis and VEGF expression in the heart and skeletal muscle of mice.
Hif1a↓,
NF-kB↓,

666- EGCG,    The Role of EGCG in Breast Cancer Prevention and Therapy
- Review, NA, NA
ROMO1↑, higher concentration and exposure time
VEGF↓,
TumCG↓,

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↓,

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↓,
EMT↓,
survivin↓,
Nanog↓,
Casp3↑,
Casp7↑,

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↑,

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↑,

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↓,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,

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↓, 94% of subjects subsequently tested negative for ENOX2 presence.

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↑, complete molecular remission 20 years after a diagnosis of chronic lymphocytic leukemia

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↑, induced cell cycle arrest in the G1 phase
Apoptosis↑,

641- EGCG,  Se,    Antioxidant effects of green tea
ROS↑, Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants. EGC and EGCG, both generate hydrogen peroxide at concentrations greater than 10 μM
H2O2↑, Adding milk to green tea decreases formation of hydrogen peroxide,
ROS⇅, Selenium could enhance anticancer activity of green tea [29], possibly by enhancing antioxidant activity [30, 31], or even its pro-oxidant activity [32].

642- EGCG,    Prooxidant Effects of Epigallocatechin-3-Gallate in Health Benefits and Potential Adverse Effect
ROS↑, under high-dose conditions. Autooxidation of EGCG generates substantial ROS
H2O2↑, One EGCG molecule could produce more than two H2O2 molecules
Apoptosis↑,
Trx↓, High concentration of EGCG inactivated Trx/TrxR via the formation of EGCG-Trx1 and EGCG-TrxR conjugates
TrxR↓, High concentration of EGCG inactivated Trx/TrxR via the formation of EGCG-Trx1 and EGCG-TrxR conjugates
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↓, EGCG inhibits activities of EGFR, VEGFR, and IGFR
VEGFR2↓,
IGFR↓,
Ca+2↑, EGCG elevates cytosolic Ca2+ levels
NO↑, EGCG-stimulated elevation of cytosolic calcium contributes to NO production by binding to calmodulin
Sp1/3/4↓,
NF-kB↓,
AP-1↓,
STAT1↓,
STAT3↓,
FOXO↓, FOXO1
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↑, Without oxygen, EGCG in aqueous solution was rather stable
pH↓, acidic environments enhance the stability of EGCG

646- EGCG,  PI,    Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice
- in-vivo, Nor, NA
*BioAv↑, area under the curve (AUC) by 1.3-fold compared to mice treated with EGCG only

647- EGCG,    Food Inhibits the Oral Bioavailability of the Major Green Tea Antioxidant Epigallocatechin Gallate in Humans
- Human, Nor, NA
*BioAv↑, taking EGCG capsules without food was better; the AUC was 2.7 and 3.9 times higher than when EGCG capsules were taken with a light breakfast

693- EGCG,  CAP,  Phen,    Metabolite modulation of HeLa cell response to ENOX2 inhibitors EGCG and phenoxodiol
- in-vitro, Cerv, HeLa
ENOX2↓, all 3 are enox2 inhibitors
TumCG↓, growth was inhibited by about 70% with 50 μM EGCG and 60% by 0.5 μM phenoxodiol

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↓, ERK1/2
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↓, downregulation of the Wnt/β-catenin pathway interferes with CSC traits
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↓, MGT might similarly act as a glycolysis inhibitor
GAPDH↓,
ROS↑, Tea cathechins may act both as anti-oxidant and as pro-oxidants
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↓, identified epigallocatechin as a key compound in SS inhibiting LDH-A activity

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↓, significantly reduced lactate production
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↓, only inhibited glycolysis in cancer cells with a high rate of aerobic glycolysis (HCC-LM3 and HepG2 cells) but not in low-glycolytic cells (Huh-7 and LO2 cells).
lactateProd↓,
GlucoseCon↓,
TumCP↓,
TumCCA↑, arrests cells in S Phage
Casp3↑, citrate enhanced the EGCG upregulation of active caspase-3 and cleaved-PARP in both HCC-LM3 and HepG2 cells
cl‑PARP↑,
Apoptosis↑,
Casp8↑,
Casp9↑,
Cyt‑c↝, translocation of cytochrome c from the mitochondria into the cytosol
MMP↓,
BAD↑,
GLUT2↓, figure2 c,d
PKM2∅, figure2 c,d

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↓, EGCG inhibits cyclooxygenase-2 without affecting COX-1 expression at both the mRNA and protein levels, in androgen-sensitive LNCaP and androgen-insensitive PC-3
*antiOx↑, EGCG is a well-known antioxidant and it scavenges most free radicals, such as ROS and RNS
Hif1a↓,
NF-kB↓,
VEGF↓,
STAT3↓,
Bcl-2↓,
P53↑, EGCG activates p53 in human prostate cancer cells
Akt↓,
p‑Akt↓,
p‑mTOR↓,
EGFR↓,
AP-1↓,
BAX↑,
ROS↑, apoptosis was convoyed by ROS production and caspase-3 cleavage
Casp3↑,
Apoptosis↑,
NRF2↑, pancreatic cancer cells via inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling
*H2O2↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*NO↓, EGCG plays a role in the inhibition of H2O2 and NO production in human skin [10].
*SOD↑, fig 2
*Catalase↑, fig 2
*GPx↑, fig 2
*ROS↓, fig 2

674- EGCG,    Biocompatible and biodegradable nanoparticles for enhancement of anti-cancer activities of phytochemicals
- Review, Var, NA
*BioEnh↑, Liposomes, micelles, nanoemulsions, solid lipid nanoparticles improve bioavialability

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↓,
STAT3↓,
TumCCA↑, EGCG causes cell cycle arrest by preventing cyclin accumulation D1
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↑, EGCG promoted G1 phase arrest
P53↑,
ERK↓, EGCG inactivated ERK1/2 protein kinases
EGFR↓,
p‑ERK↑,
VEGF↓,
Hif1a↓,
miR-203↓, in CA33 cells only
miR-210↑,

671- EGCG,    The Epigenetic Modification of Epigallocatechin Gallate (EGCG) on Cancer
other↝, multiple effects exerted by EGCG in cancer is the epigenetic change by DNA methylation or methyltransferases, histone acetylation or deacetylases, and no coding RNAs (micoRNAs).

672- EGCG,    Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer
- Review, NA, NA
DNMT1↓,
HDAC↓, HDAC1, HDAC2
G9a↓,
PRC2↓,
DNMT3A↓,
67LR↓, anti-proliferative action of EGCG is mediated by the binding to 67LR, whose expression is increased in tumour cells.
Apoptosis↑,
TumCCA↑,

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↑, TfR being upregulated and FtH being down-regulated
FTH1↓,

684- EGCG,    Improving the anti-tumor effect of EGCG in colorectal cancer cells by blocking EGCG-induced YAP activation
- in-vitro, CRC, NA
eff↑, YAP blockade increases the sensitivity of CRC cells to EGCG treatment
Akt↓,
VEGFR2↓,
STAT3↓,
P53↓,
Hippo↓,
YAP/TEAD↑, activates downstream YAP : Activation of YAP impedes the anti-tumor effects of EGCG

675- EGCG,    When Natural Compounds Meet Nanotechnology: Nature-Inspired Nanomedicines for Cancer Immunotherapy
- Review, Var, NA
*BioAv↑, (NPs)-based delivery strategies

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↑, IRE1 α
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↑, Delayed cancer onset, Prevention of colorectal adenoma recurrence
TumMeta↓,
YMcells↑, from 0.43 kPa to 2.53 kPa, about 6.2-fold
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↑,

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↓, significantly inhibited the activities and mRNA levels of the glycolytic enzymes hexokinase (HK)
LDHA↓,
Hif1a↓,
GLUT1↓,
TumVol↓,
VEGF↓,

682- EGCG,    Suppressive Effects of EGCG on Cervical Cancer
- Review, NA, NA
E7↓,
E6↓,
PI3K/Akt↓,
P53↑,
p27↑,
P21↑,
CDK2↓,
mTOR↓,
HIF-1↓,
IGF-1↓,
EGFR↓,
ERK↓, ERK1/2
VEGF↓,

683- EGCG,    Targeting the AMP-Activated Protein Kinase for Cancer Prevention and Therapy
- Review, NA, NA
AMPK↑, EGCG analogs activate AMPK
TumCP↓,
P21↑,
mTOR↓,
COX2↓,

1292- Ge,  EGCG,    Antiproliferative and Apoptotic Effects Triggered by Grape Seed Extract (GSE) versus Epigallocatechin and Procyanidins on Colon Cancer Cell Lines
- in-vitro, Colon, Caco-2 - in-vitro, CRC, HCT8
TumCG↓, growth inhibition induced by Italia and Palieri grape seed extracts was significantly higher than that it has been recorded with epigallocatechin, procyanidins and their association
Apoptosis↑, apoptosis induced by Italia, Palieri and Red Globe grape seed extracts was considerably higher than has been recorded with epigallocatechin, procyanidins

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.

81- QC,  EGCG,    Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
- in-vivo, Pca, NA
COMT↓,
MRP1↓,
Ki-67↓,
Bax:Bcl2↑,
AR↓,
Akt↓,
p‑ERK↓, ERK1/2
COMT↓,
eff↑, Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea

77- QC,  EGCG,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, CD44+ - in-vitro, NA, CD133+ - in-vitro, NA, PC3 - in-vitro, NA, LNCaP
Casp3↑,
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Vim↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF1/TCF
TCF↓, LEF1/TCF
Nanog↓,

74- QC,  EGCG,    Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancer
- Human, Pca, NA

60- QC,  EGCG,  isoFl,  isoFl,  isoFl  The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, pCSCs
Casp3↑,
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF-1/TCF


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 153

Results for Effect on Cancer/Diseased Cells:
67LR↓,1,   ACSL4↑,1,   AFP↓,1,   Akt↓,8,   p‑Akt↓,3,   ALC↓,1,   AMPK↑,4,   p‑AMPK↑,1,   angioG↓,3,   AntiAg↑,3,   AP-1↓,4,   Apoptosis↑,22,   AR↓,4,   aSmase↑,1,   ATF4↑,4,   ATG5↑,1,   ATG5↝,1,   ATP↓,1,   ATP↝,1,   BAD↓,1,   BAD↑,2,   Bak↑,3,   BAX↑,9,   BAX⇅,1,   Bax:Bcl2↑,3,   BBB↑,1,   Bcl-2↓,12,   Bcl-xL↓,4,   Beclin-1↑,1,   Beclin-1↝,1,   BID↓,1,   BioAv↓,1,   BioAv∅,1,   BMI1↓,1,   Ca+2↑,1,   Ca+2↝,1,   cardioP↑,2,   Casp↑,2,   Casp3↑,15,   cl‑Casp3↑,1,   Casp7↑,5,   Casp8↓,1,   Casp8↑,6,   Casp9↑,6,   CD133↓,1,   CD24↓,1,   CD44↓,1,   CDK2↓,2,   CDK4↓,1,   CDK6↓,1,   Ceru↓,1,   chemoP↑,1,   ChemoSen↑,2,   CHOP↑,2,   cMyc↓,1,   cognitive↑,1,   COMT↓,3,   COX1↓,1,   COX2↓,5,   CSCs↓,3,   CTR1↑,1,   cycD1↓,2,   cycE↓,1,   Cyt‑c↑,4,   Cyt‑c↝,1,   Diablo↑,1,   DNAdam↑,2,   DNMT1↓,5,   DNMT3A↓,2,   DNMTs↓,6,   Dose?,2,   Dose↑,1,   Dose↝,1,   Dose∅,1,   E6↓,1,   E7↓,1,   ECAR↓,2,   eff↓,5,   eff↑,15,   EGF↓,1,   EGFR↓,9,   eIF2α↓,1,   eIF2α↑,2,   EMT↓,5,   ENOX2↓,4,   ER Stress↑,6,   ER-α36↓,2,   ERK↓,8,   ERK↑,1,   p‑ERK↓,1,   p‑ERK↑,1,   EZH2↓,2,   FAK↓,2,   Fas↑,1,   Fenton↑,2,   Ferroptosis↑,1,   FGF↓,1,   FOXO↓,1,   FOXO↑,1,   FTH1↓,1,   G9a↓,1,   GAPDH↓,1,   GDH↓,1,   Gli↓,1,   Gli1↓,5,   GLI2↓,1,   GlucoseCon↓,4,   GLUT1↓,1,   GLUT2↓,1,   GLUT3↑,1,   GlutMet↓,1,   Glycolysis↓,8,   GPx↑,2,   GPx4↓,1,   GRP78/BiP↓,1,   GRP78/BiP↑,5,   H2O2↑,4,   H3↓,1,   ac‑H3↑,2,   ac‑H4↑,1,   Half-Life↝,1,   Half-Life∅,1,   HATs↓,2,   HDAC↓,7,   HDAC1↓,3,   HDAC2↓,1,   HDAC3↓,1,   HDAC4↓,1,   HER2/EBBR2↓,2,   HGF/c-Met↓,2,   HH↓,5,   HIF-1↓,1,   Hif1a↓,10,   Hippo↓,1,   HK2↓,6,   HK2∅,1,   HO-1↓,1,   HO-1↑,2,   HSP27↓,1,   hTERT↓,2,   IGF-1↓,3,   IGF-1R↑,1,   IGFR↓,1,   p‑IGFR↓,1,   IL1β↓,1,   IL6↓,3,   IL8↓,1,   IRE1↑,2,   Iron↑,1,   IronCh↑,2,   ITGB3↓,1,   IκB↓,1,   IκB↑,1,   JAK↓,1,   JNK↓,1,   JNK↑,1,   Jun↓,1,   JWA↑,1,   Keap1↓,2,   Ki-67↓,5,   KRAS↓,1,   lactateProd↓,5,   LC3B↑,1,   LC3II↑,2,   LDHA↓,4,   LDHA∅,1,   LEF1↓,2,   Let-7↑,1,   lipoGen↓,1,   MAPK↓,4,   Mcl-1↓,1,   MCP1↓,1,   MDA↑,1,   MDM2↓,1,   MDM2↑,1,   miR-145↑,1,   miR-200c↑,1,   miR-203↓,1,   miR-21↓,1,   miR-210↓,1,   miR-210↑,1,   miR-330-5p↑,1,   miR-34a↑,1,   MMP↓,5,   MMP↑,1,   MMP-10↓,1,   MMP2↓,4,   MMP2⇅,1,   MMP7↓,1,   MMP9↓,4,   MMP9↑,1,   MMP9⇅,1,   MMPs↓,4,   MRP1↓,1,   mtDam↑,3,   mTOR↓,6,   p‑mTOR↓,1,   Myc↓,1,   NADH↑,1,   NADHdeh?,1,   Nanog↓,3,   necrosis↑,1,   NF-kB↓,16,   NF-kB↑,1,   NO↑,1,   NOS2↓,1,   NOTCH↓,1,   NOTCH1↓,1,   NOTCH3↓,1,   NQO1↑,1,   NQO2↑,1,   NRF2↓,1,   NRF2↑,6,   NRF2⇅,1,   OCR↓,1,   OCT4↓,1,   OS↑,2,   other↑,3,   other↝,2,   other∅,1,   OXPHOS↓,2,   P-gp↓,1,   p16↑,2,   P21↑,8,   p27↑,3,   p38↓,1,   p38↑,1,   p50↓,1,   P53↓,1,   P53↑,9,   PARP↑,5,   cl‑PARP↑,2,   PARP16↓,1,   PCNA↓,2,   PD-L1↓,1,   PDGF↓,1,   p‑PDGF↓,1,   PDGFR-BB↑,1,   PDHA1↓,1,   PERK↑,2,   p‑PERK↓,1,   PFK↓,3,   PFKP↓,1,   pH↓,1,   PI3K↓,2,   PI3K/Akt↓,3,   PI3k/Akt/mTOR↓,1,   PKA↓,1,   PKM2↓,2,   PKM2∅,1,   cl‑PPARα↓,1,   pRB↑,1,   p‑pRB↓,2,   PRC2↓,1,   Prx↓,1,   PSA↓,1,   PTCH1↓,3,   PTCH2↓,1,   PTEN↑,4,   Pyruv↓,1,   RadioS↑,1,   Raf↓,1,   RANTES?,1,   RAS↓,1,   RECK↑,1,   Remission↓,1,   Remission↑,4,   RNS↓,1,   ROMO1↑,1,   ROS↓,2,   ROS↑,24,   ROS⇅,1,   mt-ROS↓,1,   RPSA↓,1,   SCF↓,1,   selectivity↑,7,   Shh↓,1,   SK↓,1,   Slug↓,3,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   SMAD4↓,1,   Smo↓,4,   Snail↓,3,   SOD↑,1,   SOD1↓,1,   SOD1↑,1,   Sp1/3/4↓,3,   Sp1/3/4↑,1,   STAT↓,1,   STAT1↓,1,   STAT3↓,6,   survivin↓,6,   SUZ12↓,1,   TCF↓,2,   Telomerase↓,3,   TfR1/CD71↑,1,   TGF-β↓,2,   TIMP1↑,1,   TIMP2↑,1,   TIMP3↑,1,   TNF-α↓,4,   TOP1↑,1,   TOP2↑,1,   toxicity∅,1,   TP53↓,1,   TP53↑,1,   Trx↓,2,   Trx1↓,1,   TrxR↓,2,   TumAuto↑,5,   TumCCA?,1,   TumCCA↑,8,   TumCD↓,1,   TumCG↓,9,   TumCI↓,5,   TumCMig↓,4,   TumCP↓,12,   tumCV↓,1,   TumMeta↓,2,   TumVol↓,3,   TumW↓,2,   UHRF1↓,1,   uPA↓,2,   uPA↝,1,   UPR↓,1,   UPR↑,5,   VEGF↓,11,   VEGFR2↓,2,   Vim↓,3,   Warburg↓,1,   Weight∅,1,   Wnt↓,3,   Wnt↑,1,   XBP-1↑,1,   XIAP↓,5,   YAP/TEAD↑,1,   YMcells↑,1,   Zeb1↓,2,   Zeb1↑,1,   β-catenin/ZEB1↓,7,   γH2AX↑,1,  
Total Targets: 342

Results for Effect on Normal Cells:
ACTA2↓,1,   angioG↑,1,   AntiAg↑,1,   AntiCan↑,1,   antiOx?,1,   antiOx↑,6,   AP-1↓,1,   Apoptosis↓,3,   ASC↓,1,   Aβ↓,2,   BAX↓,1,   BBB↑,1,   BioAv↓,2,   BioAv↑,6,   BioAv↝,1,   BioEnh↑,7,   Ca+2?,1,   Ca+2↓,2,   i-Ca+2↓,1,   cardioP↑,4,   Casp1↓,2,   Casp12↓,1,   Casp3↓,1,   Catalase↑,4,   CHOP↓,1,   cognitive↑,1,   COL1A1↓,1,   COX2↓,1,   cycD1↓,1,   Cyt‑c↓,1,   DNMTs↓,1,   Dose↝,2,   Dose∅,1,   E2Fs↑,1,   eff↓,1,   ER Stress↓,1,   FOXO1↑,1,   GDH↓,1,   Gli1↑,1,   glucose↓,1,   GPx↑,1,   GR↑,1,   GRP78/BiP↓,2,   GSH↑,1,   GSTA1↑,1,   GSTs↑,1,   H2O2↓,1,   H2O2↑,1,   Half-Life↝,1,   HDAC↓,2,   HDAC↑,1,   HDAC1↓,1,   hepatoP↓,1,   HO-1↑,3,   IGF-1R↓,1,   IL1↓,1,   IL18↓,1,   IL1β↓,1,   IL6↓,3,   IL8↓,1,   Inflam↓,3,   iNOS↓,1,   IRE1↓,1,   JAK↓,1,   LDH↓,1,   LDL↓,1,   lipid-P↓,1,   MDA↓,1,   memory↑,1,   MMP↑,1,   MMP2↓,2,   MPO↓,1,   n-MYC↑,1,   neuroG↑,1,   neuroP↑,3,   NF-kB↓,2,   NLRP3↓,2,   NO↓,2,   NQO1↑,1,   Nrf1↑,1,   NRF2↓,1,   NRF2↑,7,   other↓,1,   other↑,1,   P53↓,1,   p‑PARP↓,1,   PDGFR-BB↓,1,   PERK↓,1,   PGC-1α↓,1,   PGC-1α↑,1,   PGC1A↑,1,   PKM2↑,1,   radioP↑,1,   RenoP↑,1,   Rho↓,2,   RNS↓,1,   ROS↓,10,   Shh↑,1,   SIRT1↑,2,   SOD↑,5,   SOD1↑,1,   SOD2↑,1,   SREBP2↓,1,   TCF-4↓,1,   TNF-α↓,3,   TOP2↑,1,   toxicity↓,1,   toxicity↑,1,   toxicity∅,2,   Trx1↑,1,   TXNIP↓,1,   UPR↓,2,   VEGF↓,1,   α-SMA↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 115

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:73  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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