EGCG (Epigallocatechin Gallate) / Apoptosis Cancer Research Results

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

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

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

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

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

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

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

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

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

-Note half-life 3–5 hours.
- low BioAv 1%? despite its limited absorption, it is rapidly disseminated throughout the body
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Does NOT Lower AntiOxidant defense in Cancer Cells: NRF2↑, TrxR↓**, SOD, GSH Catalase HO1 GPx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, Notch↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective(possible damage at high dose), CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

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


Apoptosis, Apoptosis: Click to Expand ⟱
Source:
Type: type of cell death
Situation in which a cell actively pursues a course toward death upon receiving certain stimuli.
Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die.
Scientific Papers found: Click to Expand⟱
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↓, p‑PERK↓, Apoptosis↑, eIF2α↓, UPR↓, ER Stress↑, eff↑, GRP78/BiP↓,
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↑, ROS↑, Apoptosis↑, ER Stress↑, *Inflam↓, *cardioP↑, *antiOx↑, *LDL↓, *NF-kB↓, *MPO↓, *glucose↓, *ROS↓, ATG5↑, LC3B↑, MMP↑, lactateProd↓, VEGF↓, Zeb1↑, Wnt↑, IGF-1R↑, Fas↑, Bak↑, BAD↑, TP53↓, Myc↓, Casp8↓, LC3II↑, NOTCH3↓, eff↑, p‑Akt↓, PARP↑, *Cyt‑c↓, *BAX↓, *memory↑, *neuroP↑, *Ca+2?, GRP78/BiP↑, CHOP↑, 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↓, *ROS↓, *Apoptosis↓, *GRP78/BiP↓, *CHOP↓, *PERK↓, *IRE1↓, *p‑PARP↓, *Casp3↓, *Casp12↓, *ER Stress↓, *UPR↓,
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↓, ER Stress↑, GRP78/BiP↑, PERK↑, eIF2α↑, ATF4↑, IRE1↑, Apoptosis↑, Casp3↑, Casp7↑, Wnt↓, β-catenin/ZEB1↓, *toxicity∅, UPR↑,
1516- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*Dose∅, Half-Life∅, BioAv∅, BBB↑, toxicity∅, eff↓, Apoptosis↑, Casp3↑, Cyt‑c↑, cl‑PARP↑, DNMTs↓, Telomerase↓, angioG↓, Hif1a↓, NF-kB↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, IGF-1↓, H3↓, HDAC1↓, *LDH↓, *ROS↓,
1974- EGCG,    Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes
- in-vitro, Nor, NA
*ROS↓, *NO↓, *MMP↑, *i-Ca+2↓, *HO-1↑, *Catalase↑, *NRF2↑, *Trx1↑, *antiOx↑, *SOD↑, *Apoptosis↓,
2395- EGCG,    EGCG inhibits diabetic nephrophathy through up regulation of PKM2
- Study, Diabetic, NA
*PKM2↑, *Apoptosis↓, *PGC-1α↑,
3236- EGCG,  Buty,    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↑, TumCCA?, HDAC1↓, DNMT1↓, survivin↓, HDAC↓, P21↑, NF-kB↑, γH2AX↑, ac‑H3↑, DNAdam↑,
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↓, mtDam↑, Apoptosis↑, ATP↓, lipoGen↓, eff↑,
3243- EGCG,    (−)-Epigallocatechin-3-Gallate Inhibits Colorectal Cancer Stem Cells by Suppressing Wnt/β-Catenin Pathway
CD133↓, CSCs↓, TumCP↓, Apoptosis↑, Wnt↓, β-catenin/ZEB1↓,
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↑, *toxicity↓, *eff↓,
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↑, TumVol↓,
25- EGCG,  QC,    Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
COMT↓, TumCP↑, TumCCA↑, Apoptosis↑,
640- EGCG,    Epigallocatechin Gallate (EGCG) Is the Most Effective Cancer Chemopreventive Polyphenol in Green Tea
- in-vitro, CRC, HCT116 - in-vitro, Colon, SW480
TumCCA↑, Apoptosis↑,
642- EGCG,    Prooxidant Effects of Epigallocatechin-3-Gallate in Health Benefits and Potential Adverse Effect
ROS↑, H2O2↑, Apoptosis↑, Trx↓, TrxR↓, JNK↑, HO-1↑, Fenton↑,
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↓,
691- EGCG,    Preclinical Pharmacological Activities of Epigallocatechin-3-gallate in Signaling Pathways: An Update on Cancer
- Review, NA, NA
Apoptosis↑, necrosis↑, TumAuto↑, ERK↓, p38↓, NF-kB↓, VEGF↓,
692- EGCG,    EGCG: The antioxidant powerhouse in lung cancer management and chemotherapy enhancement
- Review, NA, NA
ROS↑, Apoptosis↑, DNAdam↑, CTR1↑, JWA↑, β-catenin/ZEB1↓, P53↑, Vim↓, VEGF↓, p‑Akt↓, Hif1a↓, COX2↓, ERK↓, NF-kB↓, Akt↓, Bcl-xL↓, miR-210↓,
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↑,
989- EGCG,  Citrate,    In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity
- in-vitro, HCC, NA - in-vivo, NA, NA
PFK↓, Glycolysis↓, lactateProd↓, GlucoseCon↓, TumCP↓, TumCCA↑, Casp3↑, cl‑PARP↑, Apoptosis↑, Casp8↑, Casp9↑, Cyt‑c↝, MMP↓, BAD↑, GLUT2↓, PKM2∅,
20- EGCG,    Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer
- in-vivo, Liver, NA - in-vivo, Tong, NA
HH↓, Gli1↓, Smo↓, TNF-α↓, COX2↓, *antiOx↑, Hif1a↓, NF-kB↓, VEGF↓, STAT3↓, Bcl-2↓, P53↑, Akt↓, p‑Akt↓, p‑mTOR↓, EGFR↓, AP-1↓, BAX↑, ROS↑, Casp3↑, Apoptosis↑, NRF2↑, *H2O2↓, *NO↓, *SOD↑, *Catalase↑, *GPx↑, *ROS↓,
672- EGCG,    Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer
- Review, NA, NA
DNMT1↓, HDAC↓, G9a↓, PRC2↓, DNMT3A↓, 67LR↓, Apoptosis↑, TumCCA↑,
676- EGCG,  Chemo,    The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review
- Review, NA, NA
PI3k/Akt/mTOR↓, Apoptosis↑, ROS↑, TumAuto↑,
677- EGCG,    Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2 α /ATF4 and IRE1 α
- in-vitro, CRC, HT-29
ER Stress↑, GRP78/BiP↑, PERK↑, eIF2α↑, ATF4↑, IRE1↑, Apoptosis↑,
4682- EGCG,    Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
- Review, Var, NA
CSCs↓, EMT↓, ChemoSen↑, CD133↓, CD44↓, ALDH1A1↓, Nanog↓, OCT4↓, TumCP↓, Apoptosis↑, p‑GSK‐3β↓, GSK‐3β↑, β-catenin/ZEB1↓, cMyc↓, XIAP↓, Bcl-2↓, survivin↓, Vim↓, Slug↓, Snail↓,
4681- EGCG,    Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling
- in-vitro, Ovarian, ES-2
TumCP↓, Apoptosis↑, Nanog↓, SOX2↓, Fibronectin↓, CD133↓,
1292- GSE,  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↓, Apoptosis↑,
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↓, *toxicity↑, Dose?, eff↓, eff↓,
60- QC,  EGCG,  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↓, CSCs↓, Apoptosis↑, TumCMig↓, TumCI↓, CD44↓, CD133↓,

Showing Research Papers: 1 to 29 of 29

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 29

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   H2O2↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↑, 6,   Trx↓, 1,   TrxR↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   MMP↑, 1,   mtDam↑, 1,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 2,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 1,   lactateProd↓, 2,   lipoGen↓, 1,   PFK↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2∅, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 3,   Apoptosis↑, 26,   BAD↑, 2,   Bak↑, 2,   BAX↑, 2,   Bcl-2↓, 5,   Bcl-xL↓, 2,   Casp3↑, 6,   Casp7↑, 2,   Casp8↓, 1,   Casp8↑, 2,   Casp9↑, 1,   Cyt‑c↑, 1,   Cyt‑c↝, 1,   Fas↑, 1,   JNK↑, 1,   JWA↑, 1,   Myc↓, 1,   necrosis↑, 1,   p38↓, 1,   survivin↓, 4,   Telomerase↓, 1,   TumCD↓, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   ac‑H3↑, 1,   PRC2↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↓, 1,   eIF2α↑, 2,   ER Stress↑, 4,   GRP78/BiP↓, 1,   GRP78/BiP↑, 3,   IRE1↑, 2,   PERK↑, 2,   p‑PERK↓, 1,   UPR↓, 1,   UPR↑, 2,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMT1↓, 2,   DNMT3A↓, 1,   DNMTs↓, 1,   G9a↓, 1,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 2,   TP53↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA?, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD133↓, 4,   CD44↓, 2,   CSCs↓, 3,   EMT↓, 3,   ERK↓, 2,   Gli1↓, 1,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 2,   HDAC1↓, 2,   HH↓, 1,   IGF-1↓, 1,   IGF-1R↑, 1,   p‑mTOR↓, 1,   Nanog↓, 3,   NOTCH3↓, 1,   OCT4↓, 2,   PTEN↑, 1,   Smo↓, 1,   SOX2↓, 1,   STAT3↓, 1,   TCF↓, 1,   TumCG↓, 1,   Wnt↓, 2,   Wnt↑, 1,  

Migration ⓘ

67LR↓, 1,   AP-1↓, 1,   Fibronectin↓, 1,   LEF1↓, 1,   MMPs↓, 1,   Slug↓, 3,   Snail↓, 3,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 5,   TumCP↑, 1,   Vim↓, 2,   Zeb1↓, 1,   Zeb1↑, 1,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 3,   EGFR↓, 1,   Hif1a↓, 3,   miR-210↓, 1,   VEGF↓, 4,  

Barriers & Transport ⓘ

BBB↑, 1,   CTR1↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   NF-kB↓, 4,   NF-kB↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

COMT↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv∅, 1,   ChemoSen↑, 1,   Dose?, 1,   eff↓, 4,   eff↑, 3,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   Myc↓, 1,   TP53↓, 1,  

Functional Outcomes ⓘ

PARP16↓, 1,   toxicity∅, 1,   TumVol↓, 1,  
Total Targets: 145

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 1,   H2O2↓, 1,   HO-1↑, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 5,   SOD↑, 2,   Trx1↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,   LDH↓, 1,   LDL↓, 1,   PKM2↑, 1,  

Cell Death ⓘ

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

Protein Folding & ER Stress ⓘ

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

DNA Damage & Repair ⓘ

p‑PARP↓, 1,  

Migration ⓘ

Ca+2?, 1,   Ca+2↓, 1,   i-Ca+2↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose∅, 1,   eff↓, 1,  

Clinical Biomarkers ⓘ

LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,   toxicity↓, 1,   toxicity↑, 1,   toxicity∅, 1,  
Total Targets: 43

Scientific Paper Hit Count for: Apoptosis, Apoptosis
29 EGCG (Epigallocatechin Gallate)
2 Quercetin
2 Resveratrol
1 Butyrate
1 Folic Acid, Vit B9
1 Gold NanoParticles
1 Curcumin
1 Sulforaphane (mainly Broccoli)
1 Genistein (soy isoflavone)
1 Aflavin-3,3′-digallate
1 Citric Acid
1 Chemotherapy
1 Grapeseed extract
1 Luteolin
1 Apigenin (mainly Parsley)
1 isoflavones
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#:14  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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