EGCG (Epigallocatechin Gallate) / Casp3 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

Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱

Source:

Type:

Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.

Scientific Papers found: Click to Expand⟱

3201-

EGCG,

Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential

Review,

NA,

*AntiCan↑, *cardioP↑, *neuroP↑, *BioAv↝, *BioAv↓, *BioAv↓, *Dose↝, *Half-Life↝, *BioAv↑, *BBB↑, *hepatoP↓, *other↓, *Inflam↓, *NF-kB↓, *AP-1↓, *iNOS↓, *COX2↓, *ROS↓, *RNS↓, *IL8↓, *JAK↓, *PDGFR-BB↓, *IGF-1R↓, *MMP2↓, *P53↓, *NRF2↑, *TNF-α↓, *IL6↓, *E2Fs↑, *SOD1↑, *SOD2↑, Casp3↑, Cyt‑c↑, PARP↑, DNMTs↓, Telomerase↓, Hif1a↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, TumCP↓, MAPK↓, HGF/c-Met↓, TIMP1↑, HDAC↓, MMP9↓, uPA↓, GlutMet↓, ChemoSen↑, chemoP↑,

3203-

EGCG,

(-)- Epigallocatechin-3-gallate induces GRP78 accumulation in the ER and shifts mesothelioma constitutive UPR into proapoptotic ER stress

NA,

MM,

ROS↑, Ca+2↝, GRP78/BiP↑, ATF4↑, XBP-1↑, CHOP↑, Casp3↑, Casp8↑, *GRP78/BiP↓, *UPR↓, UPR↑,

3205-

EGCG,

The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas

Review,

Var,

Review,

AD,

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,

*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↑,

1303-

EGCG,

(-)-Epigallocatechin-3-gallate induces apoptosis in human endometrial adenocarcinoma cells via ROS generation and p38 MAP kinase activation

in-vitro,

EC,

TumCP↓, ER-α36↓, cycD1/CCND1↓, ERK↑, Jun↓, BAX↑, Bcl-2↓, cl‑Casp3↑, ROS↑, p38↑,

1516-

EGCG,

Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential

Review,

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↓,

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

50-100uM

ROS↑, MMP↓, Casp3↑, Cyt‑c↑, Trx1↓, Ceru↓, IL6↓, IL8↓, MCP1↓, RANTES?, uPA↝, ROS↑,

3238-

EGCG,

Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications

Review,

Var,

Telomerase↓, DNMTs↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, HATs↓, HDAC↓, selectivity↑, uPA↓, NF-kB↓, TNF-α↓, *ROS↓, *antiOx↑, Hif1a↓, VEGF↓, MMP2↓, MMP9↓, FAK↓, TIMP2↑, Mcl-1↓, survivin↓, XIAP↓, PCNA↓, p16↑, P21↑, p27↑, pRB↑, P53↑, MDM2↑, ROS↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Diablo↑, BAX⇅, cl‑PPARα↓, PDGF↓, EGFR↓, FOXO↑, AP-1↓, JNK↓, COX2↓, angioG↓,

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+

 20-60 uM

HH↓, Smo↓, PTCH1↓, PTCH2↓, Gli1↓, GLI2↓, Gli↓, Bcl-2↓, XIAP↓, Shh↓, survivin↓, Casp3↑, Casp7↑, CSCs↓, Nanog↓, cMyc↓, OCT4↓, EMT↓, Snail↓, Slug↓, Zeb1↓, TumCMig↓, TumCI↓, eff↑,

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

25–100 μM

Casp8↑, Casp9↑, Casp3↑, BAX↑, PARP↑, TumVol↓, NF-kB↓, MMP9↓,

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,

EGCG (50 μM), citrate (5 mM)

in-vivo,

NA,

10 mg/kg/ BW/day

mice

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,

in-vivo,

Tong,

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↓,

668-

EGCG,

The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer Treatment

Review,

BC,

MCF-7

Review,

BC,

MDA-MB-231

HER2/EBBR2↓, EGFR↓, mtDam↑, ROS↑, PI3K/Akt↓, P53↑, P21↑, Casp3↑, Casp9↑, BAX↑, PTEN↑, Bcl-2↓, hTERT/TERT↓, STAT3↓, TumCCA↑, Hif1a↓,

681-

EGCG,

Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical models

vitro+vivo,

BC,

10-320 μM

Casp3↑, Casp8↑, Casp9↑, TumAuto↑, Beclin-1↝, ATG5↝, GlucoseCon↓, lactateProd↓, ATP↝, HK2↓, LDHA↓, Hif1a↓, GLUT1↓, TumVol↓, VEGF↓,

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+

 20 uM

 CD44+ and CD133+ CSCs can be isolated from PC-3 and LNCaP

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↓, TCF↓, eff↑, CSCs↓, TumCG↓, tumCV↓,

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

 20 uM

Casp3↑, Casp7↑, Bcl-2↓, survivin↓, XIAP↓, EMT↓, Slug↓, Snail↓, β-catenin/ZEB1↓, LEF1↓, CSCs↓, Apoptosis↑, TumCMig↓, TumCI↓, CD44↓, CD133↓,

Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

chemoP↑, 1, toxicity∅, 1, TumVol↓, 2,
Total Targets: 166

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, Catalase↑, 1, GPx↑, 1, H2O2↓, 1, MPO↓, 1, NRF2↑, 1, RNS↓, 1, ROS↓, 6, SOD↑, 1, SOD1↑, 1, SOD2↑, 1,

Core Metabolism/Glycolysis ⓘ

glucose↓, 1, LDH↓, 1, LDL↓, 1,

Cell Death ⓘ

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

Transcription & Epigenetics ⓘ

other↓, 1,

Protein Folding & ER Stress ⓘ

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

DNA Damage & Repair ⓘ

P53↓, 1, p‑PARP↓, 1,

Cell Cycle & Senescence ⓘ

E2Fs↑, 1,

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,

Migration ⓘ

AP-1↓, 1, Ca+2?, 1, Ca+2↓, 1, MMP2↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1, PDGFR-BB↓, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

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

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

IL6↓, 1, LDH↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 2, hepatoP↓, 1, memory↑, 1, neuroP↑, 2, toxicity∅, 1,
Total Targets: 59

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3

17 EGCG (Epigallocatechin Gallate)
2 Quercetin
1 Citric Acid
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#:42  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

EGCG (Epigallocatechin Gallate) / Casp3 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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