EGCG (Epigallocatechin Gallate) / CSCs Cancer Research Results

EGCG, EGCG (Epigallocatechin Gallate): Click to Expand ⟱

Features:

Epigallocatechin-3-gallate — EGCG is a naturally occurring galloylated flavan-3-ol and the quantitatively dominant catechin in green tea leaves from Camellia sinensis. It is formally classified as a dietary polyphenol, catechin and investigational pleiotropic bioactive compound. EGCG has concentration-, oxidation-, metal- and cellular-context-dependent activity: it can function as an antioxidant and NRF2-associated cytoprotective agent in normal tissues, but may generate reactive oxygen species and induce stress-mediated death in susceptible cancer cells. It is not an approved anticancer drug, and purified high-dose extracts are pharmacologically and toxicologically distinct from brewed green tea.

Primary mechanisms (ranked):

Biphasic redox modulation, including direct radical scavenging and metal chelation at lower exposure, but auto-oxidation, hydrogen-peroxide generation and pro-oxidant stress under permissive cancer-cell culture conditions.
Suppression of proliferative and survival signalling, particularly PI3K–AKT–mTOR, NF-κB, receptor tyrosine kinase, STAT and context-dependent MAPK pathways.
Mitochondrial dysfunction and intrinsic apoptosis through mitochondrial membrane-potential loss, cytochrome-c release and caspase activation.
Cell-cycle arrest through modulation of cyclins, cyclin-dependent kinases, p21, p27 and p53-associated signalling.
Inhibition of invasion, epithelial–mesenchymal transition and extracellular-matrix degradation through reduced FAK, MMP-2, MMP-9, uPA and related motility pathways.
Suppression of HIF-1α–VEGF signalling, angiogenesis and hypoxia adaptation.
Metabolic disruption involving reduced glycolysis, glucose transport and context-dependent mitochondrial energy production.
Epigenetic modulation, including experimental inhibition or altered expression of DNMTs, HDACs and EZH2.
Modulation of proteostasis, autophagy, endoplasmic-reticulum stress and unfolded-protein responses.
NRF2 activation as a secondary adaptive mechanism, generally cytoprotective in normal cells but potentially protective or treatment-resistant in some cancers.
Chemosensitization or radiosensitization in selected experimental models; treatment protection, antagonism or normal-tissue radioprotection can also occur depending on dose, schedule and therapy.

Bioavailability / PK relevance: Oral bioavailability is low and highly variable because EGCG is chemically unstable near neutral or alkaline pH, has limited intestinal permeability, undergoes extensive methylation, glucuronidation and sulfation, and is influenced by food and microbiota. Plasma concentrations after tea consumption are usually submicromolar, while large supplemental doses may transiently produce low-micromolar exposure. Fasting can increase systemic exposure but may also increase hepatic toxicity risk. Nanoencapsulation, lipid carriers and other delivery systems improve exposure experimentally but are not established anticancer treatments.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM EGCG, whereas conventional oral administration generally produces submicromolar to low-micromolar plasma concentrations. Thus, many direct cytotoxic, glycolytic, mitochondrial and kinase effects occur at concentrations substantially exceeding typical achievable systemic exposure. EGCG can also oxidize in culture media and generate extracellular hydrogen peroxide, creating experimental effects that may not translate directly in vivo.

Clinical evidence status: Extensive preclinical evidence; multiple small human biomarker, prevention and early-phase studies; limited randomized evidence for selected premalignant or recurrence-prevention settings; no established therapeutic efficacy against active cancer and no regulatory approval as an anticancer agent. A recent randomized colorectal adenoma study reported reduced recurrence, but this does not establish treatment efficacy for invasive colorectal cancer. Ongoing clinical studies continue to investigate prevention and adjunctive applications.

Safety and interactions: Brewed green tea is generally well tolerated, whereas concentrated green-tea extracts and purified EGCG have been associated with dose-dependent aminotransferase elevations and rare clinically significant liver injury. Doses around 800 mg EGCG per day have generated a regulatory safety signal, and a universally safe supplemental dose has not been established. Risk may be higher with fasting administration, pre-existing liver disease or multi-ingredient weight-loss products. EGCG can bind non-heme iron, alter drug transporters or metabolic enzymes, and modify exposure to some medications; oncology use should therefore be reviewed for drug-specific interactions.

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). FDA says <800mg/day (hepatotoxicity)
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

EGCG Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Biphasic redox modulation	↑ ROS or ↓ ROS (dose-dependent) (context-dependent)	↓ ROS; ↑ antioxidant buffering	P–R	Oxidative stress or antioxidant protection	Auto-oxidation and metal-catalysed peroxide formation may drive cancer-cell toxicity; culture-medium oxidation can exaggerate this mechanism.
2	PI3K AKT mTOR survival signalling	↓ PI3K; ↓ AKT; ↓ mTOR	↔ or adaptive modulation	R–G	Reduced proliferation and survival	Frequently reported across models, but direct target engagement at physiologically achievable concentrations remains uncertain.
3	Mitochondrial apoptosis	↓ ΔΨm; ↑ cytochrome c; ↑ caspase-9; ↑ caspase-3; ↑ PARP cleavage	↔ or preserved mitochondrial function	R–G	Intrinsic apoptotic death	Usually downstream of redox stress, calcium disturbance or survival-pathway inhibition.
4	NF-κB inflammatory survival signalling	↓ NF-κB; ↓ COX-2; ↓ inflammatory cytokines	↓ pathological inflammation	R–G	Reduced inflammatory and anti-apoptotic transcription	Potentially relevant to tumour-promoting inflammation and treatment resistance.
5	Cell-cycle regulation	↓ cyclin D1; ↓ cyclin E; ↓ CDK2; ↓ CDK4; ↓ CDK6; ↑ p21; ↑ arrest	↔ or transient arrest	G	Cytostatic growth inhibition	Arrest may occur at G1, S or G2/M depending on tumour type and concentration.
6	Invasion EMT and matrix remodelling	↓ EMT; ↓ FAK; ↓ uPA; ↓ MMP-2; ↓ MMP-9; ↓ migration	↔	G	Reduced invasion and metastatic phenotype	Predominantly supported by cellular and animal models.
7	HIF-1α VEGF angiogenesis axis	↓ HIF-1α; ↓ VEGF; ↓ angiogenic signalling	↔ or context-dependent vascular protection	G	Reduced hypoxia adaptation and angiogenesis	Responses depend on oxygen tension, cell type and exposure.
8	Glycolysis and energy metabolism	↓ GLUT1; ↓ HK2; ↓ PKM2; ↓ LDHA; ↓ ECAR; ↓ ATP (model-dependent)	↔ or improved metabolic homeostasis	R–G	Metabolic stress	Many metabolic findings use concentrations above typical human plasma exposure.
9	Calcium ER stress and proteostasis	↑ Ca²⁺; ↑ ER stress; ↑ UPR; ↑ GRP78 (context-dependent)	↔ or ↓ pathological ER stress	P–G	Proteotoxic stress and apoptosis	GRP78 and UPR activation may promote death or adaptation depending on intensity and duration.
10	Epigenetic regulation	↓ DNMT activity; ↓ HDAC signalling; ↓ EZH2 (model-dependent)	↔	G	Re-expression of suppressed genes	Biochemical inhibition and intracellular effects may require different concentrations.
11	NRF2 antioxidant response	↑ NRF2 or ↔ (context-dependent)	↑ NRF2; ↑ HO-1; ↑ GSH; ↑ antioxidant enzymes	R–G	Secondary adaptive cytoprotection	NRF2 can protect normal tissue but may also counteract EGCG-induced oxidative injury or support resistant cancer cells.
12	Cancer stemness signalling	↓ Wnt β-catenin; ↓ Hedgehog GLI; ↓ Notch; ↓ stem-cell markers	↔	G	Reduced self-renewal phenotype	Evidence remains predominantly preclinical and model-dependent.
13	Chemosensitization	↑ treatment response or ↓ resistance (drug-dependent)	↔ or ↑ tissue protection	R–G	Adjunctive modulation	Reported with several cytotoxic and targeted agents, but EGCG can also alter drug absorption, transport or stability; combinations require individual evaluation.
14	Radiosensitization and radioprotection	↑ radiosensitivity or ↔ (schedule-dependent)	↓ radiation injury in some models	R–G	Context-dependent radiation modulation	Opposing tumour and normal-tissue effects are possible; clinical evidence is insufficient for routine supplementation during radiotherapy.
15	Clinical Translation Constraint	Effective experimental exposure often not systemically achievable	↑ hepatic risk with concentrated high-dose extracts	G	Limited clinical translation	Poor oral bioavailability, rapid metabolism, instability, formulation heterogeneity, fasting-related exposure, liver toxicity and limited definitive oncology trials constrain deployment.

P: 0–30 min R: 30 min–3 hr G: >3 hr

Alzheimer’s disease relevance: EGCG has substantial preclinical neuroprotective evidence but no established clinical efficacy for Alzheimer’s disease. Proposed actions include inhibition or remodelling of amyloid-β aggregation, altered amyloid precursor protein processing, metal chelation, reduced tau-associated injury, suppression of neuroinflammation, mitochondrial protection and activation of NRF2-associated antioxidant defences. Most positive findings derive from biochemical, cellular or animal models, and brain exposure after conventional oral administration is uncertain. EGCG should therefore be classified as preclinical or exploratory for Alzheimer’s disease rather than as a validated disease-modifying therapy.

EGCG in Alzheimer’s Disease

Rank	Pathway / Axis	Modulation	Primary Effect	Notes / Interpretation
1	Amyloid beta aggregation	↓ fibril formation; ↑ non-toxic aggregate remodelling	Reduced amyloid-associated toxicity	Strong biochemical and preclinical rationale; effective brain exposure in humans remains uncertain.
2	Amyloid precursor protein processing	↑ non-amyloidogenic processing; ↓ amyloidogenic burden (model-dependent)	Reduced amyloid generation	Primarily demonstrated in cellular and animal systems.
3	Neuroinflammation	↓ NF-κB; ↓ NLRP3; ↓ inflammatory cytokines; ↓ microglial activation	Reduced inflammatory neurotoxicity	Inflammatory effects are context-, model- and dose-dependent.
4	Oxidative stress and NRF2	↓ ROS; ↑ NRF2; ↑ HO-1; ↑ endogenous antioxidant defence	Neuronal cytoprotection	Antioxidant signalling is more relevant at achievable exposure than many direct cytotoxic cancer mechanisms.
5	Mitochondrial function	↑ membrane stability; ↑ ATP preservation; ↓ mitochondrial ROS	Improved neuronal bioenergetics	Supported mainly by experimental injury and transgenic models.
6	Tau pathology	↓ tau phosphorylation or aggregation (model-dependent)	Reduced cytoskeletal and synaptic injury	Less developed evidence base than amyloid-related mechanisms.
7	Metal homeostasis	↓ redox-active iron and copper interactions	Reduced metal-promoted aggregation and oxidative injury	Chelation may contribute mechanistically but could also impair dietary non-heme iron absorption.
8	Clinical Translation Constraint	↓ oral and brain exposure; ↑ formulation variability	Uncertain human efficacy	No convincing evidence currently establishes EGCG as an Alzheimer’s disease-modifying treatment.

CSCs, Cancer Stem Cells: Click to Expand ⟱

Source:

Type:

Cancer Stem Cells

Phytochemicals (natural plant-derived compounds) that may affect CSCs:
Curcumin
— suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Resveratrol
— shown to reduce CSC populations and sphere formation in multiple models.
Sulforaphane (from broccoli sprouts)
— reported to inhibit CSC properties and pathways; active in vitro and in vivo.
EGCG (epigallocatechin-3-gallate, green tea)
— reduces CSC markers and sphere formation in several cancer types.
Quercetin
— reported to inhibit CSC proliferation, self-renewal and invasiveness (breast, endometrial, others).
Berberine
— shown to suppress CSC “stemness” and reduce tumorigenic properties in multiple models.
Genistein (soy isoflavone)
— decreases CSC markers, sphere formation and stemness signaling in prostate/breast/other models.
Honokiol (Magnolia bark)
— shown to eliminate or suppress CSC-like populations in oral, colon, glioma models.
Luteolin
— inhibits stemness/EMT and reduces CSC markers and self-renewal in breast, prostate and other models.
Withaferin A (from Withania somnifera / ashwagandha)
— multiple preclinical reports show WA targets CSCs and reduces tumor growth/metastasis in models.

Circadian disruption in cancer and regulation of cancer stem cells by circadian clock genes: An updated review
Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy
Can we utilise the circadian clock to target cancer stem cells?

Scientific Papers found: Click to Expand⟱

4656-

CUR,

EGCG,

Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signaling

in-vitro,

BC,

MDA-MB-231

 curcumin (10 μM) with/without EGCG (10 μM) for 48 hours.

in-vitro,

BC,

MCF7

CSCs↓, Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44) positive cell population.
CD44↓,
p‑STAT3↓, curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained.
NF-kB↓, Notably, curcumin is a potent inhibitor of NFκB
TumCI↓, Wound-healing assay revealed that curcumin and EGCG suppress cell invasiveness

5397-

CUR,

SFN,

RES,

EGCG,

Ash

Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential

Review,

Var,

CSCs↓, curcumin, sulforaphane, resveratrol, EGCG, genistein, quercetin, parthenolide, berberine, and withaferin A. Collectively, these compounds suppress CSC self-renewal,

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↓,

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↓, EGCG also inhibited the components of Shh pathway (smoothened, patched, Gli1 and Gli2)
Smo↓,
PTCH1↓,
PTCH2↓,
Gli1↓,
GLI2↓,
Gli↓,
Bcl-2↓, inhibiting the expression of Bcl-2 and XIAP, and activating caspase-3
XIAP↓,
Shh↓,
survivin↓,
Casp3↑,
Casp7↑,
CSCs↓, EGCG inhibited the expression of pluripotency maintaining transcription factors (Nanog, c-Myc and Oct-4), and self-renewal capacity of pancreatic CSCs.
Nanog↓,
cMyc↓,
OCT4↓,
EMT↓, EGCG inhibited EMT by inhibiting the expression of Snail, Slug and ZEB1, and TCF/LEF transcriptional activity,
Snail↓,
Slug↓,
Zeb1↓,
TumCMig↓, significantly reduced CSC’s migration and invasion, suggesting the blockade of signaling involved in early metastasis.
TumCI↓,
eff↑, combination of quercetin with EGCG had synergistic inhibitory effects on self-renewal capacity of CSCs through attenuation of TCF/LEF and Gli activities

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,

NOTCH1↓, Furthermore, EGCG suppressed Notch1
BMI1↓,
SUZ12↓,
EZH2↓,
miR-34a↑,
miR-200c↑,
miR-145↑,
CSCs↓, (EGCG), an active catechin present in green tea, has been shown to suppress CSC growth in various cancers

4680-

EGCG,

The Potential of Epigallocatechin Gallate in Targeting Cancer Stem Cells: A Comprehensive Review

Review,

Var,

CSCs↓, major bioactive green tea polyphenol (-)-epigallocatechin gallate (EGCG) has been fruitful in downgrading cancer stemness signaling and CSC biomarkers in cancer progression.
EMT↓, Cancer stemness is intricately related to epithelial-mesenchymal transition (EMT), metastasis and therapy resistance, and EGCG has been evidenced to regress all these CSC-related effects
TumMeta↓,
RadioS↑, By inhibiting CSC characteristics EGCG has also been evidenced to sensitize the tumor cells to radiotherapy and chemotherapy.
ChemoSen↑,
BioAv↓, concern about its bioavailability, stability and efficacy against spheroids raised from parental cells. Therefore, novel nano formulations of EGCG and adjuvant therapy of EGCG with other phytochemicals or drugs or small molecules may have a better pr

4682-

EGCG,

Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate

Review,

Var,

CSCs↓, EGCG inhibits the transcription and translation of genes encoding stemness markers, indicating that EGCG generally inhibits the self-renewal of CSCs.
EMT↓, EGCG inhibits the expression of the epithelial-mesenchymal transition phenotypes of human CSCs.
ChemoSen↑, Green tea prevents human cancer, and the combination of EGCG and anticancer drugs confers cancer treatment with tissue-agnostic efficacy.
CD133↓, CD133, CD44, ALDH1A1, Nanog, Oct4
CD44↓,
ALDH1A1↓,
Nanog↓,
OCT4↓,
TumCP↓, These results show that EGCG inhibits proliferation and induces apoptosis of lung CSCs
Apoptosis↑,
p‑GSK‐3β↓, EGCG (0–100 μM) inhibited the phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser 9, which significantly increases the expression of GSK3β, and decreases the expression of β-catenin and its downstream target gene c-Myc.
GSK‐3β↑,
β-catenin/ZEB1↓,
cMyc↓,
XIAP↓, EGCG (30–60 μM) inhibits the expression of X-linked inhibitor of apoptosis protein (XIAP), Bcl2, and survivin as well as that of the EMT markers vimentin, Slug, Snail, and nuclear β-catenin.
Bcl-2↓,
survivin↓,
Vim↓,
Slug↓,
Snail↓,

4683-

EGCG,

Epigallocatechin-3-gallate inhibits self-renewal ability of lung cancer stem-like cells through inhibition of CLOCK

in-vitro,

Lung,

A549

in-vitro,

Lung,

H1299

in-vivo,

Lung,

A549

<span class="wphighlight">CSCs</span> nude mouse xenograft model

CSCs↓, it was demonstrated that EGCG suppressed the CSC-like characteristics of lung cancer cells by targeting CLOCK.
CD133↓, EGCG also decreased the ratio of CD133+ cells
CLOCK↓, The Wnt/β-catenin pathway was notably inactivated by the knockdown of CLOCK in A549 and H1299 sphere cells.
Wnt↓, Wnt/β-catenin signaling is blocked by the knockdown of CLOCK in lung CSCs
β-catenin/ZEB1↓,
CD44↓, EGCG decreased CD133, CD44, Sox2, Nanog, and Oct4 protein expression levels by targeting CLOCK
SOX2↓,
Nanog↓,
OCT4↓,

4684-

EGCG,

EGCG inhibits CSC-like properties through targeting miR-485/CD44 axis in A549-cisplatin resistant cells

in-vivo,

NSCLC,

A549

miR-485↑, (EGCG), a green tea polyphenol which has been identified as an effective anticancer compound was able to increase miR-485 expression dose-dependently in A549/CDDP cells.
CSCs↓, in vivo experiments were employed to confirm that EGCG restrained CSC-like characteristics by increasing miR-485 and decreasing CD44 expression.
CD44↓,

4685-

EGCG,

Epigallocathechin gallate, polyphenol present in green tea, inhibits stem-like characteristics and epithelial-mesenchymal transition in nasopharyngeal cancer cell lines

in-vitro,

NPC,

TW01

in-vitro,

NPC,

TW06

CSCs↓, EGCG potently inhibited sphere formation and can eliminate the stem cell characteristics of NPC and inhibit the epithelial-mesenchymal transition (EMT) signatures.
EMT↓,
TumCMig↓, Inhibition on NPC sphere-derived cell colony formation, migration, and invasion by EGCG
TumCI↓,
OCT4↓, EGCG inhibited the expression of Klf-4 and Oct-4 in sphere-derived cells.
Snail↓, EGCG significantly inhibited the levels of Snail, Vimentin and increased E-Cadherin expression in a dose-dependent manner
Vim↓,
E-cadherin↓,
HSP70/HSPA5↓, EGCG suppresses the expression of HSP70 and HSP90, and exhibits anti-tumor activity in vitro and in vivo
HSP90↓,
AntiTum↓,

4664-

GEN,

CUR,

RES,

EGCG,

SFN

Targeting cancer stem cells by nutraceuticals for cancer therapy

Review,

Var,

CSCs↓, we will describe the some natural chemopreventive agents that target CSCs in a variety of human malignancies, including soy isoflavone, curcumin, resveratrol, tea polyphenols, sulforaphane, quercetin, indole-3-carbinol, 3,3′-diindolylmethane, withafe
other↝, Because chemotherapy and radiotherapy cannot effectively remove CSCs
eff↑, Curcumin and EGCG combination attenuated the CD44+ cell population via inhibition of pSTAT3 and retaining the crosstalk between STAT3 and NF-κB in breast cancer cells [233]
CD44↓,
p‑STAT3↓,

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+ <span class="wphighlight">CSCs</span> can be isolated from PC-3 and LNCaP

in-vitro,

NA,

CD133+

in-vitro,

NA,

PC3

in-vitro,

NA,

LNCaP

Casp3↑, EGCG induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2, survivin and XIAP in CSCs.
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓, EGCG inhibits epithelial-mesenchymal transition by inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF
Vim↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF1/TCF
TCF↓, LEF1/TCF
eff↑, inhibition of Nanog by shRNA enhanced the inhibitory effects of EGCG
CSCs↓, prostate cancer cell lines contain a small population of CD44+CD133+ cancer stem cells and their self-renewal capacity is inhibited by EGCG.
TumCG↓, EGCG inhibits the growth of cancer stem cells isolated from human prostate cancer cell lines
tumCV↓, EGCG inhibits the formation of primary and secondary tumor spheroids and cell viability of human prostate cancer stem cells

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↑, EGCG induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2, survivin and XIAP in CSCs.
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF-1/TCF
CSCs↓, quercetin synergizes with EGCG in inhibiting the self-renewal properties of prostate CSCs, inducing apoptosis, and blocking CSC's migration and invasion.
Apoptosis↑,
TumCMig↓,
TumCI↓,
CD44↓, EGCG inhibits the self-renewal capacity of CD44+α2β1+CD133+ CSCs isolated from human primary prostate tumors,
CD133↓,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

AntiTum↓, 1,
Total Targets: 67

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: CSCs, Cancer Stem Cells

15 EGCG (Epigallocatechin Gallate)
3 Curcumin
2 Sulforaphane (mainly Broccoli)
2 Resveratrol
2 Quercetin
1 Ashwagandha(Withaferin A)
1 5-fluorouracil
1 Genistein (soy isoflavone)
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#:795  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

EGCG (Epigallocatechin Gallate) / CSCs Cancer Research Results

EGCG Mechanistic Profile

EGCG in Alzheimer’s Disease

Pathway results for Effect on Cancer / Diseased Cells:

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

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