Cancer preventive and therapeutic effects of EGCG, the major polyphenol in green tea

Figures & data

Fig. 1 Schematic drawing of green tea leaves composition.

Table 1 Dried green tea composition.

Molecular group	Component		Molecular Formula	MW (g/mol)	Percent of dried tea extract	Main Biological effects
Polyphenols	Catechins	Epicatechin	C15H14O6	290.26	30–42	Cancer prevention, antioxidant, antibacterial and antiviral effects.
		Epicatechin-3-gallate	C22H18O10	442.37
		Epigallocatechin	C15H14O7	306.27
		Epigallocatechin-3-gallate (EGCG)	C22H18O11	458.375
	Flavonols	Kaempferol	C15H10O6	286.23	5–10	Anti-histamine and anti-inflammatory effects.
		Quercetin	C15H10O7	302.236
		Myricetin	C15H10O8	318.2351
	Depsides	Theogallin	C14H16O10	344.27	2–4	Inhibition of Influenza A viruses.
		Chlorogenic acid	C16H18O9	354.31
		Coumarylquinic acid	C16H18O8	338.312
Organic acids	Ascorbic acid		C6H8O6	176.124	1–2	Anticancer effects.
	Gallic acid		C7H6O5	170.12	0.5
	Quinic acid		C7H12O6	192.17	2
	Folic acid		C19H19N7O6	441.404	0.5
	Other organic acids		–	–	4–5
Amino acids	Theanine		C7H14N2O3	174.2	4–6	Neuronal cell protection and relaxation effect.
	γ-aminobutyric acid		C4H9NO2	103.121	2–4	Decrease of blood pressure.
Methylxanthines	Caffeine		C8H10N4O2	194.19	7–10	Increased alertness and a mild diuretic effects.
	Theobromine		C7H8N4O2	180.164
	Theophylline		C7H8N4O2	180.167
Carbohydrates	Glycosides		–	–	10–15	Energy and prevent blood sugar increase.
Minerals	Aluminium, fluorine, manganese, iron, magnesium, potassium, phosphorus, zinc, selenium and sodium.		–	–	6–8	Regulators.
Volatiles	Saponin		C58H94O27	1223.363	0.02–1	Anti-fungal, anti-inflammatory, and anti-allergy properties.
	Linalool		C10H18O	154.25
	△-Cardinene		C15H24	204.357
	Geraniol		C10H18O	154.253
	Nerolidol		C15H26O	222.37
	α-Terpineol		C10H18O	154.25
	Cis-Jasmone		C11H16O	164.246
	Indole		C8H7N	117.15
	β-Inone		C13H20O	192.302
	1-Octanal		C8H16O	128.215
	Indole-3-Carbinol		C9H9NO	147.18
	β-Caryophyllene		C15H24	204.36
Vitamins	Thiamine (B1)		C12H17N4OS^+	265.355	–	Maintenance of healthy skin and mucus membrane.
	Riboflavin (B2)		C17H20N4O6	376.369
	Niacin (B3)		C6H5NO2	123.111
	Vitamin B6		C8H11NO3	169.18
	Vitamin E		C29H50O2	430.717
	β-Carotene		C40H56	536.888
Chlorophyll	–		C55H72O5N4Mg	893.509	–	Deodorizing effect, kidney stone prevention and strengthens immune system.

Fig. 2 Molecular structure green tea catechins.

Fig. 3 Schematic drawing of the regulative actions of EGCG. This carton is based on the available literature about the anticancer effects of EGCG.

Fig. 4 Schematic drawing of the regulative actions of EGCG combined with other dietary and pharmaceutical agents. This carton is based on the available literature.

Table 2 Compounds have previously combined with EGCG.

		Molecular structure	Molecular Formula	MW (g/mol)	Cancers (cell lines)
[6]-Gingerol			C17H26O4	294.391	Glioma (SW1783, LN18 and 1321N1) [30]
Arginine			C6H14N4O2	174.204	Prostate (PC-3, LNCaP and DU-145) [44] and bladder (T-24) [137] cancers
Ascorbic acid			C6H8O6 or HC6H7O6	176.124
Curcumin			C21H20O6	368.385	Breast (MDA-MB-231 [31] and MCF-7 [125,146] ), lung (A549 [45] and NCI-H460 [45]), prostate (PC-3) [33] and nsophageal (TE-8 and SKGT-4) [32] cancers
Green tea polyphenols (GTP)	Epicatechin		C15H14O6	290.26	Prostate (LNCaP) cancer[147]
	Epicatechin-3-gallate		C22H18O10	442.37
	Epigallocatechin		C15H14O7	306.27
	Kaempferol		C15H10O6	286.23
	Quercetin		C15H10O7	302.236	Prostate (PC-3 [33] and LNCaP [33] [147]) cancer
	Myricetin		C15H10O8	318.2351	Prostate (LNCaP) cancer [147]
	Theogallin		C14H16O10	344.27
	Chlorogenic acid		C16H18O9	354.31
	Coumarylquinic acid		C16H18O8	338.312
GS			C31H28O12	592.553	Colorectal (HCT-116 and SW480) cancer[128]
Polyphenon E	Caffeine		C8H10N4O2	194.194	Lung cancer [148]
	(+)-Gallocatechin		C15H14O7	306.27
	EGC
	(+−)-Catechin		C15H14O6	290.271
	EC
	(−)-Gallocatechin gallate		C22H18O11	458.375
	ECG
	(−)-Catechin gallate		C22H18O10	442.376
	EGCG
pterostilbene			C16H16O3	256.301	Pancreatic (PANC-1 and MIA-Pa-Ca-2) cancer [36]
Sulforaphane			C6H11NOS2	177.28	Prostate (PC-3) cancer [34]
Tocotrienol-rich fraction (TRF)			C28H42O2	410.642	Glioma (1321N1, LN18 and SW1783) [30]
TRAIL		–	–	–	Pancreatic (MIA-Pa-Ca-2) cancer [74]

Table 3 Anticancer effects of EGCG alone and combination.

Cancers	Cell lines	EGCG Combination	Dose & IC50	Biological effects
Breast cancer	MDA-MB-231	EGCG	50 and 100 μM [149]; 50 and 80 μg/mL [75]; 20, 40 and 60 μM [150]; 10 and 20 μM [110]; 0.01–1000 μM [151]. IC50: 50 μM (24 h) [149], 15.7 μM [151]	Inhibits cell proliferation and viability through suppression of Wnt signaling via inducing the HBP1 transcriptional repressor [149], epigenetic repression of hTERT [150] and inhibition of glucose uptake and metabolism [151]. Induces cell apoptosis through stimulation of pro-apoptotic signaling and downregulation of MMP-9 expression [75]. Inhibits cell invasion, motility and migration through inhibition of EGF-induced MMP-9 via suppressing FAK and ERK signaling pathways [110].
		pEGCG	20 μM [150]; 50 μmol/L [79]	Inhibit cell proliferation via Epigenetic repression of hTERT [150]. In addition, it inhibits significantly tumor growth in vivo associated with increased proteasome inhibition and apoptosis induction in tumor tissues [79].
		EGCG + Curcumin	E (20,25,35 and 40 μM) and/or C (2,3,4 and 6 μM)	Inhibits cancer proliferation in vitro and in xenograft mouse models through inhibition of VEGFR-1, EGFR and AKT protein level [31].
		EGCG (E) + Vitexin-2-O-xyloside (X) + Raphasatin (G)	E (10,20,30,40,50 μg/mL), × (30,50,80, 100,120 μg/mL) and/or G (5,10,15,30,50 μg/mL). IC50: E (135 ± 16), X (158 ± 13), G (36 ± 5) μg/mL	Mixture activates ROS mediated mitochondrial pathway causing G0/G1 cell cycle arrest and induces apoptosis [46].
		EGCG-Ptx-PLGA-Casein-NPs	–	Induce apoptosis, inhibite NF-κB activation and downregulate the key genes associated with angiogenesis, tumor metastasis and survival [141].
		EGCG-LbL-PSS/PAH-NPs	1 or 5 μM [152]	Inhibit HGF-induced c-Met signaling after prolonged pre-incubation [13,152] .
	MCF-7	EGCG	10, 20, 30, 40 and 50 [73]; 10, 25, 50 and 100 [109]; 1 and 10 μM [153]; 20, 40 and 60 [150]; 0.01–1000 μM [151]; 10, 20 and 40 μM [154]; 0.1, 1, 10, 50 and 100 μM [146]. IC50: 50 μg/mL [73,109] ; 44.1 μM [151] 40 μM [154]; 19–20 μM [146]	Induces growth inhibition and apoptosis through surviving expression downregulation via suppressing AKT pathway and activation of caspase-9 [73]. Inhibits cell migration and invasion through downregulation of VASP expression and Rac1 activity [109]. Inhibits nicotine and estradiol-induced cell proliferation via downregulation of α9-nicotinic acetylcholine receptor signaling pathway [153]. Inhibits cell viability and proliferation through epigenetic repression of hTERT [150], inhibition of glucose uptake and metabolism [151], epigenetic downregulation of ER-α via p38MAPK/CK2 activation [154] and activation of Cav3.2 channels via elicit of Ca2 + spike [146].
		pEGCG	20 μM [150]	Inhibit cell proliferation via epigenetic repression of hTERT [150]
		EGCG + Curcumin	E (2, 4, 10, 20, 40, 100) μM + C 20 μM	Induce growth inhibition and apoptosis through upregulation of caspase-dependent apoptotic signaling pathways and inhibition of P-glycoprotein pump function [125].
		EGCG (E) + Vitexin-2-O-xyloside (X) + Raphasatin (G)	E (10,20,30,40,50 μg/mL), X (30,50,80, 100,120 μg/mL) and G (5,10,15,30,50 μg/mL); IC50: E (135 ± 16), X (158 ± 13), G (36 ± 5) μg/mL	Mixture activates ROS mediated mitochondrial pathway causing G0/G1 cell cycle arrest and induces apoptosis [46].
	Hs578T	EGCG	10 μM	Inhibits cell proliferation and migration trough downregulation of VEGF expression [155].
	T47D	EGCG	10, 20 and 40 μM. IC50: 40 μM	Inhibits cell proliferation trough epigenetic downregulation of ER-α via p38MAPK/CK2 activation [154].
	NF639	EGCG	20, 40, 60 and 80 µg/mL [156]; 40 μg/mL [108]	Inhibits Her-2/Neu signaling, proliferation, and transformed phenotype of the Cancer Cells [156]. Inhibit branching colony growth and cell invasion through induction of estrogen receptor α expression via activating FOXO3a signaling [108].
	4 T1	EGCG	10 mg/kg, IP injection on day 7, 9 and 11	Suppresses tumor growth in vivo by inhibiting tumor-associated macrophage infiltration and M2 polarization [157].
	ALDH1^+ in SUM-149 and SUM-190 stem cells	EGCG	20, 40, 80 and 120 μg/mL	Inhibits growth of cancer stem cells in vitro and in vivo. Inhibits spheroid formation and induces apoptosis [133].
	CD44^+/CD24^− in MDA-MB-231 and MDA-MB-436 stem cells	EGCG	20, 30 and 40 μM	Inhibits tumorsphere formation and reduces cancer stem cell population through downregulation of estrogen receptor-α36, EGFR, p-ERK1/2 and p-AKT [158].
Lung Cancer	A549	EGCG	40–300 μM, IC50: 265 ± 7.1 μM (24 h) in vitro and 40 mg/kg/week by IP injection into BALB/c nude female mice for 33 days [101]. 50 and 100 μM in vitro and 0.05% in drinking water into BALB/c nude male mice for 21 days [102]. 1, 5, 10, 20 and 40 μM [159]. 10, 25, 50 and 100 [104,105] . 10–40 μM [86]. 80 μM [160]. 25 and 100 [161]. 100 μM into flanks of nude mice [103^[104]–105] . 5,10,25 and 50 [162]	Induces cell apoptosis through inhibition of FASN activity and EGFR signaling pathway [101]. Reduces xenograft tumor growth and angiogenesis in vivo [101,102] through inhibiting of oncogene and IGF-1via suppressing HIF-1α and VEGF protein expression [103,104] . Inhibits cell proliferation through upregulation of endostatin expression and suppression of VEGF expression [102] and suppressing of the expression of the cell death-inhibiting gene, Bcl-xL [161]. Inhibits cell growth through induction of G0/G1 cell cycle arrest via inhibiting EGFR/cyclin D1 signaling [86] and upregulation of miR-210 expression via stabilizing HIF-1α [162]. Inhibits the anchorage-independent growth of cancer cells, induces p53 accumulation and upregulates its target genes, promotes the stability of p53 and MDM2, promotes nuclear localization and activity of p53, inhibits proteasomal degradation-dependent p53 ubiquitination and inhibits the interaction of p53 and MDM2 [159]. Inhibits HPV-16 oncoprotein induced angiogenesis conferred by cancer cells through the inhibition of HIF-1a protein expression and HIF-1a dependent expression of VEGF, IL-8, and CD31 as well as activation of Akt [104]. Inhibits cancer chemo-resistant variants through downregulation of Axl and Tyro 3 expression [160]. Inhibits nicotine-induced migration, invasion and upregulation of HIF-1α, VEGF, COX-2, p-Akt and p-ERK [105].
		EGCG + Curcumin	10,20,40 μM EGCG and/or the same concentrations for curcumin in vitro while fourteen 3 to 4-week old female BALB/c nude mice were i.p. implanted with 5 × 106 A549 cells. At the third day after the A549 cells injected, the mice were randomized into two groups (7 mice/group) and treated with control (NS, 100 mL/kg) or EGCG and curcumin (20 mg/kg, respectively) [45]	Inhibit cell growth in vitro and in vivo through induction of cell cycle arrest at G1 and S/G2 phases via downregulating cyclin D1 and cyclin B1 [45].
	CL13	EGCG	5,10,25 and 50	Suppresses cancer cell growth through upregulating miR-210 expression caused by stabilizing HIF-1α [162].
		EGCG + N-acetylcysteine (NAC)	(0–100) μM of EGCG in the presence or absence of 0–2 mM NAC.	EGCG and NAC interact to form EGCG-2′-NAC adduct which induces cell culture apoptosis [126].
	H1299	EGCG	10,20,30,40 and 50 μM in vitro, 0.1, 0.3 and 0.5% in diets and 30 mg/kg/d by IP injection into male NCr nu/nu mice for 45 days. IC50: 20 μM in vitro and 0.15 μM in vivo [163]; 5,10,25 and 50 [162]	Inhibits cancer growth in vivo and in vitro and induces ROS and cell apoptosis [163]. Suppresses cancer cell growth through upregulating miR-210 expression caused by stabilizing HIF-1α [162].
	H460	EGCG	1,5,10,20 and 40 μM [159]. 10–40 μM [86]. 80 μM [160]. 5,10,25 and 50 [162]	Inhibits the anchorage-independent growth of cancer cells, induces p53 accumulation and upregulates its target genes, promotes the stability of p53 and MDM2, promotes nuclear localization and activity of p53, inhibits proteasomal degradation-dependent p53 ubiquitination and inhibits the interaction of p53 and MDM2[159]. Inhibits cell growth through induction of G0/G1 cell cycle arrest via inhibiting EGFR/cyclin D1 signaling [86]. Inhibit cancer cells proliferation including their chemo-resistant variants through downregulation of Axl and Tyro 3 expression [160]. Suppresses cancer cell growth through upregulating miR-210 expression caused by stabilizing HIF-1α [162].
	H1650	EGCG	1,5,10,20 and 40 μM [159]. 10–40 μM [86]	Inhibits the anchorage-independent growth of cancer cells, induces p53 accumulation and upregulates its target genes, promotes the stability of p53 and MDM2, promotes nuclear localization and activity of p53, inhibits proteasomal degradation-dependent p53 ubiquitination and inhibits the interaction of p53 and MDM2 [159]. Inhibits cell growth through induction of G0/G1 cell cycle arrest via inhibiting EGFR/cyclin D1 signaling [86].
	H1299	EGCG	5,10,50 and 100 μM [106]	Reduces cell motility in vitro wound healing assay. Increases Young’s modulus of H1299 from 1.24 to 2.25 showing a 2-fold increase in cell stiffness, i.e. rigid elasticity of cell membrane. Furthermore, inhibits high expression of vimentin and Slug in the cells at a leading edge of scratch. Induces inhibition of EMT phenotypes by alteration of membrane organization [106].
	Lu99	EGCG		Reduces cell motility in vitro wound healing assay. Increases Young’s modulus of Lu99 from 1.29 to 2.28 showing a 2-fold increase in cell stiffness, i.e. rigid elasticity of cell membrane. Furthermore, inhibits high expression of vimentin and Slug in the cells at a leading edge of scratch. Induces inhibition of EMT phenotypes by alteration of membrane organization [106].
	H69	EGCG	20,40,50,60,80,100,120,140,150 and 200 μM. IC50: ∼70 μM (24 h)	Induces cell apoptosis, reduces telomerase activity and inducts a cell-cycle block in S phase [164].
	H69VP
	NCI-H460	EGCG	10,25,50 and 100 in vitro [104]	Inhibits HPV-16 oncoprotein induced angiogenesis conferred by cancer cells through the inhibition of HIF-1a protein expression and HIF-1a dependent expression of VEGF, IL-8, and CD31 as well as activation of Akt [104].
		EGCG + Curcumin	10,20,40 μM EGCG and/or the same concentrations for curcumin	Inhibit cell growth in vitro and in vivo through induction of cell cycle arrest at G1 and S/G2 phases via downregulating cyclin D1 and cyclin B1 [45].
	–	EGCG + Polyphenon E	Benzo(a)pyrene [B(a)P]-induced lung cancer in female A/J mice (100 mg/kg).	Mixture inhibits significantly pulmonary adenoma formation and growth in vivo [148].
Pancreatic cancer	AsPC-1	EGCG	5–80 μM [48]	Induces apoptosis through cell cycle via G1 cell cycle arrest, regulation of cyclin D1, cdk4, cdk6, p21 and p27, activation of ROS-mediated, p53-indepdendent apoptosis signaling, inhibition of Ras/Raf-1/ERK1/2 signaling, induction of MEKK1, JNK1/2 and p38 MAPK activities [48].
	Hs 766 T
	PANC-1	EGCG	5–80 μM [48]
		EGCG + Pterostilbene	20, 30 and 40 μM EGCG with/without 30 μM Pterostilbene	The combination have additive, antiproliferative effects in vitro altering the apoptotic mechanisms by modulation at different points in the mechanism as well as the cell cycle arrest effect [36].
	MIA-Pa-Ca-2	EGCG	10, 100 and 1000 μM, IC50 below 50 μM [165]; 5–80 μM [48]	Induces apoptosis through cell cycle via G1 cell cycle arrest, regulation of cyclin D1, cdk4, cdk6, p21 and p27, activation of ROS-mediated, p53-indepdendent apoptosis signaling, inhibition of Ras/Raf-1/ERK1/2 signaling, induction of MEKK1, JNK1/2 and p38 MAPK activities [48]. Inhibits Hsp90 function by impairing Hsp90 association with co-chaperones resulting anti-proliferating effects [165].
		EGCG + TRAIL	50 μg/ml E+5 ng/ml T	A synergistic increase in apoptosis and cleavage of procaspase-3. Furthermore, clonogenic cell survival assay demonstrates the significant diminishment of cancer cell proliferation in the presence of both EGCG and TRAIL [74].
		EGCG + Pterostilbene	20, 30 and 40 μM EGCG with/without 30 μM Pterostilbene	The combination have additive, antiproliferative effects in vitro altering the apoptotic mechanisms by modulation at different points in the mechanism as well as the cell cycle arrest effect [36].
Ovarian cancer	SKOV3	EGCG	20,30,40 and 50 μg/mL [166]; 20,40,60,80,100 and 120 μg/mL [167]; 100 μM [107]	Inhibits cell proliferation and induces apoptosis through inhibition of cell cycle and DNA synthesis inducting NDA damage [166]. Downregulates AQP5, nuclear p65 and Iκ-Bα expressions [167]. Inhibit cell motility via suppression of Hsp90 chaperone system [107].
Oral cancer	SAS	EGCG	20 and 40 μM [168]	Provides antitumor immunity through inhibition of indoleamide 2,3-dioxygenase (IDO) expression via blocking the IFN-γ-induced JAK-PKC-δ-STAT1 signaling pathway [168].
	Cal-27
	Ca-922
	SCC-9	EGCG	5,10,15 and 20 μM in vitro; 10 and 20 mg/day/kg by oral gavage into the right front axilla of BALB/c nude mice	Inhibits invasion, epithelial-mesenchymal transition, and tumor growth through downregulation of MMP-2, uPA, p-FAK, p-Src, snail-1 and vimentin [111].
	SCC-4	EGCG	20 and 40 μM [168]; 10, 20, 50, 100, and 200 μM [169]	Provides antitumor immunity through inhibition of indoleamide 2,3-dioxygenase (IDO) expression via blocking the IFN-γ-induced JAK-PKC-δ-STAT1 signaling pathway [168]. Suppresses cell proliferation and promotes apoptosis and autophagy through upregulation of BAD, BAK, FAS, IGF1R, WNT11, and ZEB1 genes expressions and downregulation of CASP8, MYC, and TP53 [169].
	KB	EGCG	5,10,20,40,80,100,150 and 200 μM	Inhibits HGF-induced cell growth and invasion through suppression of HGF/c-Met signaling pathway [112].
	HSC-3	EGCG	20 and 40 μM [168]; 10,25,50 and 100 μM [113]	Provides antitumor immunity through inhibition of indoleamide 2,3-dioxygenase (IDO) expression via blocking the IFN-γ-induced JAK-PKC-δ-STAT1 signaling pathway [168]. Inhibits cancer invasion via repressing functional invadopodia formation [113].
	YD-10B	EGCG	10,25,50 and 100 μM in vitro; 20 mg/d/kg IP injection into the tongue of male BALB/c athymic nude mice every other day for 4 weeks	Inhibits cancer invasion in vitro and in vivo via repressing functional invadopodia formation and FAK/Src signaling [113].
Hypopharyngeal cancer	FaDu	EGCG	5,10,20,40,80,100,150 and 200 μM	Inhibits HGF-induced cell growth and invasion through suppression of HGF/c-Met signaling pathway [112].
Laryngeal cancer	SNU-899	EGCG	5,10,20,40,80,100,150 and 200 μM	Inhibits HGF-induced cell growth and invasion through suppression of HGF/c-Met signaling pathway [112].
	SNU-1066
Nasopharyngeal cancer	(Oct4^high/Nanog^high/β-catenin^high/ABCG2^high/MRP-1^high/MDR-1^high) in TW01 CSCs	EGCG+Cisplatin	(20 and 40 μM) E and/or (0.01, 0.1, 1 and 10 μg/mL) C	Mixture inhibits spheroid formation and cell viability as well as EGCG enhances chemo-sensitivity of cisplatin in vitro through downregulation of Oct4, β-Catenin, Nanog, ABCG2, MRP-1, MDR-1, p-STAT3, Bcl-2, Survivin and c-Myc [170].
	(Oct4^high/Nanog^high/β-catenin^high/ABCG2^high/MRP-1^high/MDR-1^high) in TW06 CSCs
	CNE2	EGCG + Cisplatin	EGCG (20 μM) + Cisplatin (10 μM) were injected subcutaneously into the flanks of nude mice and allowed to grow for 8 weeks	EGCG increases chemo-sensitivity of cisplatin in vivo [138].
	CD44^+ in CNE2 CSCs	EGCG	25,50 and 75 μM	Inhibits nasopharyngeal cancer stem cell self-renewal and migration and reverses the epithelial–mesenchymal transition via NF-κB p65 inactivation [138].
	C666-1	EGCG + Cisplatin	EGCG (20 μM) + Cisplatin (10 μM) were injected subcutaneously into the flanks of nude mice and allowed to grow for 8 weeks	EGCG increases chemo-sensitivity of cisplatin in vivo [138].
	CD44^+ in C666-1 CSCs	EGCG	25,50 and 75 μM	Inhibits nasopharyngeal cancer stem cell self-renewal and migration and reverses the epithelial–mesenchymal transition via NF-κB p65 inactivation [138].
Gastric cancer	BGC-823	EGCG	1.5 mg/d IP injection for 56 days	Inhibits xenograft angiogenesis and tumor growth [40].
		EGCG + Docetaxel	–
		EGCG + Capecitabine	200 mg/kg capecitabine daily by oral gavage + EGCG (IP injection of 1.5 mg EGCG daily	Inhibits xenograft angiogenesis and tumor growth [38].
	AGS	EGCG	5,10,25 and 50 μM in vitro and 50 μM EGCG + AGS cells in vivo into BALB/c nude female mice for 7 days [114]; 20,40,60,80,120 and 240 μg/mL [171]	Inhibits IL-6-induced angiogenesis in vitro and in vivo through inhibition of VEGF expression via suppressing Stat3 activity [114]. Inhibits cell proliferation and induces cell apoptosis through downregulation of Id1 expression [171].
	AZ521	EGCG	5,10,20 and 40 μM	Inhibits cell proliferation through downregulation of DEAD-box RNA helicase p68 [172].
	NUGC-3	EGCG	25,50,75 and 100 μM	Induces cell apoptosis through inhibition of survivin expression downstream of p73 [78].
	MKN-1
	MKN-28
	MKN-45
	TMK-1
	SGC-7901	EGCG	1.5 mg/d IP injection into female BALB/c nude for 28 days	Inhibit tumor growth and angiogenesis through reducing VEGF-induced endothelial cell proliferation, migration and tube formation [115].
Hepatocellular Carcinoma	Hepa 1c1c7	EGCG	100 μM	Inhibit cell motility via suppression of Hsp90 chaperone system [107].
	SMMC-7721	EGCG + Ascorbic acid	–	Mixture strongly suppress proliferation and metastasis through scavenging of reactive oxygen species [136].
	HepG2	EGCG	15,30,60,120 and 240	Induces non-apoptotic cell death via ROS-mediated lysosomal membrane permeabilization [173].
		EGCG + 5-FU	5-FU (0.05 μg) and EGCG (25 μmol)	Combination significantly decreased the viability of cells, compared with EGCG or 5-FU-treated cells [174].
	CD133 and NANOG in HepG2 cancer stem cells	EGCG	10 and 20 μM	Inhibit sphere formation through inhibition of CD133, Nanog, ABCC1, ABCG2, Nek2 and p-Akt [174].
Squamous cell carcinoma	SCC VII/SF	EGCG	5,10,20,40,80,100,150 and 200 μM in vitro; 25,50 and 75 mg/kg/day IP injection into the flank of syngeneic C3H/HeJ micefor 21 days	Inhibits HGF-induced cell growth and invasion through suppression of HGF/c-Met signaling pathway while it inhibits xenograft tumor growth in vivo via rising apoptosis [112].
Prostate cancer	PC-3	EGCG	0–50 μM. IC50 : 39.0 μM	Antiproliferative effects through ERK1/2 activation via MEK-independent, PI3-K-dependent signaling pathway [175].
			1 and 25 μM. IC50: 25 μM	Induces cell apoptosis through upregulation of caspase-9a expression [47].
		EGCG + Curcumin	50 and 100 μM E and/or 50 μM C	Induction of cell cycle arrest at both S and G2/M phases via upregulating p21 protein level [135].
		EGCG + Quercetin	80 μM EGCG and/or 10 and 20 μM Quercetin	Mixture demonstrates enhanced inhibition of cell proliferation and induction of cell apoptosis in vitro by increasing the intracellular concentration of EGCG and decreasing EGCG methylation [33].
		EGCG + Sulforaphane	20 and 100 μM E and/or 25 μM S	Reduction of cell viability via inhibition of AP-1 activation [34].
		EGCG + Ascorbic acid + Lysine + Proline + Arginine	50 microg/mL-500 μg/mL of the mixture	Combination inhibits cell proliferation and invasion through downregulation of MMP-2 and MMP-9 expressions [44].
		EGCg-^198AuNPs	single-dose intra-tumoral administration in human prostate cancer-bearing SCID mice	80% reduction of tumor volumes after 28 d demonstrating significant inhibition of tumor growth compared to controls [176].
		EGCG-LDH nanohybrids	25,50,75 and 100 μM/L; IC50: 16.66 μM/L (24 h), 15.47 μM/L (48 h), 16.33 μM/L (72 h)	Induce apoptosis within over 5-fold dose advantages compared to EGCG alone in in-vitro system [142].
		EGCG-PLA-PEG-NPs	0.7,1.37,2.74 and 5.48 μmol/L in vitro, IC50: 3.74 μmol/L (24 h); in vivo, mice each received 100 μg dissolved in PBS thrice weekly [26]	NPs enhance the bioavailability and limited unwanted toxicity of EGCG within 10-fold dose advantage [13]. In addition, induce apoptosis within remarkably significant increase in pro-apoptotic Bax with a concomitant decrease in anti-apoptotic Bcl-2, increase in PARP cleavage and marked induction of p21 and p27 [26].
		EGCG-PLGA-PEG-DCL-NPs	20 μM	In vitro, NPs enhance the anti-proliferative activity compared to the free EGCG modulating apoptosis and cell-cycle. In vivo, NPs enhance the bioavailability and limited unwanted toxicity [49].
		EGCG-PLGA-PEG-AG-NPs
	PC-3ML	EGCG + Doxorubicin	30 and 60 μM E + D in vitro; 0.14–57 mg/kg E and/or 2 mol/L–0.07 mg/kg D into immunodeficiency mice	Combination enhances the inhibition of metastatic tumor growth [41].
	(CD44^+CD133^+in PC-3) CSC	EGCG	30 and 60 μM	Inhibits growth and spheroid formation, induces apoptosis, inhibits EMT, inhibits migration and invasion and downregulates Casp3/7, Bcl-2, Survivin, XIAP, Vimentin, Slug, Snail and nuclear β-Catenin [132].
	LNCaP	EGCG	12 μM [177]; 20,40 and 80 μM [178]; 10, 20, 40, and 80 μg/mL [87]	Modulates cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G0/G1-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells [87].Inhibits cell proliferation through inhibition of PKC-α inhibition [177], prostate specific antigen (PSA) expression, AR transcriptional activity, growth of relapsing R1Ad tumors and tumor derived serum PSA in vivo [178].
		Green tea polyphenols (GTP)	10–80 μg/mL	In vitro and in vivo inhibition of testosterone-mediated induction of ornithine decarboxylase1 [147].
		EGCG + Quercetin	80 μM EGCG and/or 10 and 20 μM Quercetin	Quercetin enhances the anti-proliferative effects of EGCG and induction of cell apoptosis in vitro through increasing the intracellular concentration of EGCG and decreasing EGCG methylation [33].
		EGCG + Ascorbic acid+Lysine+Proline+Arginine	50 microg/mL–500 μg/mL of the mixture	Combination inhibits cell proliferation and invasion through downregulation of MMP-2 and MMP-9 expressions [44].
		EGCG-PLGA-PEG-DCL-NPs	20 μM	In vitro, NPs enhance the anti-proliferative activity compared to the free EGCG modulating apoptosis and cell-cycle. In vivo, NPs enhance the bioavailability and limited unwanted toxicity [49].
		EGCG-PLGA-PEG-AG-NPs
	(CD44^+CD133^+in LNCaP) CSCs	EGCG	30 and 60 μM	Inhibits growth and spheroid formation, induces apoptosis, inhibits EMT, inhibits migration and invasion and downregulates Casp3/7, Bcl-2, Survivin, XIAP, Vimentin, Slug, Snail and nuclear β-Catenin [132].
	DU-145	EGCG	5 μM; 10, 20, 40, and 80 μg/mL [87]	Modulates cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G0/G1-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells [87]. Inhibit cell motility and invasion through inhibition of c-Met signaling via altering the structure or function of lipid rafts [122].
		EGCG + Ascorbic acid + Lysine + Proline + Arginine	50 microg/mL–500 μg/mL of the mixture	Combination inhibits cell proliferation and invasion through downregulation of MMP-2 and MMP-9 expressions [44].
		EGCG-PLGA-PEG-DCL-NPs	20 μM	In vitro, NPs enhance the anti-proliferative activity compared to the free EGCG modulating apoptosis and cell-cycle. In vivo, NPs enhance the bioavailability and limited unwanted toxicity [49].
		EGCG-PLGA-PEG-AG-NPs
	CWR22R	EGCG	50 mg/kg/d IP injection into nude mice for 20 days.	Inhibits tumor growth and angiogenesis while promoting apoptosis of the prostate cancer cells in vivo [123].
		EGCG-P	86.7 mg/kg/d IP injection into nude mice for 20 days.	EGCG-P is more stable and effective than EGCG enhancing the inhibition of the tumor growth, angiogenesis and induces apoptosis of the prostate cancer cells in vivo [123].
	BCaPT10	EGCG	2–200 μM in vitro; 0.06% in water into male athymic mice for 1 week before xenograft surgery	Inhibits cell motility in vitro via suppression of Hsp90 molecular chaperone system which supports malignant phenotype [124].
	BCaPM-T10	EGCG	0.06% in water into male athymic mice for 1 week before xenograft surgery	Inhibits a molecular chaperone supportive of the malignant phenotype [124].
	22Rν1	EGCG-CS-NPs	3 and 6 mg/kg by oral administration into athymic nude mice for 25 days	Inhibit AR-positive 22Rν1 tumor xenograft growth and secreted prostate-specific antigen levels compared with EGCG and control groups. Significant induction of poly (ADP-ribose) polymerases cleavage, increase in the protein expression of Bax with concomitant decrease in Bcl-2, activation of caspases and reduction in Ki-67 and proliferating cell nuclear antigen [143].
	–	EGCG	Five-week-old male TRAMP offspring were fed AIN-76A diet and 0.06% EGCG in tap water for28 weeks	Inhibits cell proliferation and induces apoptosis through downregulation of AR, IGF-1, IGF-1R, p-ERK 1/2, COX-2, and iNOS [179].
	–	GTP	–	In vivo GTP oral infusion resulted in almost complete inhibition of distant site metastases. Furthermore, GTP consumption caused significant apoptosis of cancer cells causing inhibition of prostate cancer development, progression, and metastasis [127].
Melanoma	Mel 928	EGCG-CS-NPs	0.5,1.0,2.0,4.0 and 8.0 μM in vitro; IC50: 7 μM (48 h). 100 μg/mice;120 μL treatment volume into Athymic (nu/nu) male nude mice.	Induct apoptosis and cell cycle inhibition along with the growth of Mel 928 tumor xenograft. Inhibited proliferation (Ki-67 and PCNA) and induced apoptosis (Bax, PARP) in tumors harvested from the treated mice within 8-fold dose advantage of nanoformulation over native EGCG [144].
Leukemia	CEM	(MSN@EGCG)-NPs	0.4, 0.8, 1.2 and 1.6 μM in vitro and 100; NPS are i.v. injected into female Balb/c mice	Inhibit cell viability and proliferation in vitro and in vivo within a highly biocompatible and biodegradable EGCG-coated MSN nanoparticles [180].
Cervical cancer	HeLa	EGCG	10, 25, 50 and 100 μM [88]; 10,20,30,40,50,60,70,80,90 and 100 μM [85]; IC50: 47.9 μM [88]; 100 μM (24 h) and 50 μM (48 h) [85].	Cell growth inhibition trough gene expression regulation and induction of cell cycle arrest [88]. Inhibit cell proliferation, invasion and migration, and induce cell apoptosis through G1 cell cycle arrest and DNA damage, downregulation of MMP-9 gene and upregulation of TIMP-1 gene [85].
	CaSki	EGCG	10, 25, 50 and 100 μM. IC50: 27.3 μM (24 h)	Cell growth inhibition trough gene expression regulation and induction of cell cycle arrest [88].
Colorectal cancer	HCT-116	EGCG	0.05, 0.1, 0.5, 1, 5 and 10 μM [119]; 0.1, 0.5, 1, 5 and 10 μM [120]; 1, 10 and 50 μM [89]; 50 and 100 μM[181]; 12.5,25,50 and 100 μM [118]. IC50: 3 μM [119]	Suppresses cancer cells growth through cyclin D1 degradation and p21 transcriptional activation via ERK, IKK and PI3K signaling pathway [89]. Inhibits Met signaling [119] which helps to attenuate tumor spread/metastasis, independent of H2O2-related mechanisms [120]. Inhibits cell proliferation through inhibition of HGF-induced Met/ERK/AKT signaling pathway [119]and through inhibition of Akt, activation and induction of p38 MAPK activation [118]. Induces cell apoptosis through cancer-specific induction of ROS and epigenetic modulation of expression of apoptosis-related genes, such as hTERT [181].
		EGCG + Panaxadiol	E (0,10,20 and 30 μM) and/or P (0,10 and 20 μM)	Inhibit cell proliferation and induce cell cycle arrest [35].
		EGCG + EPA-FFA + GS	EGCG (0–175 μM) + EPA-FFA (0–150 μM) + GS extract (0–15 μM) for 24 h	Combination completely inhibited the mTOR signaling. Moreover, the treatment led to changes of protein translation of ribosomal proteins, c-Myc and cyclin D1. In addition, combination reduces clonal capability of cells, with block of cell cycle in G0/G1 and induction of apoptosis [128].
		EGCG + 5-FU	5-FU (0.05 μg) and EGCG (25 μmol) [174]; 25–400 μM of EGCG and/or 2.5–40 μM 5-FU [37].	Combination significantly decreased the viability of cells, compared with EGCG or 5-FU-treated cells [174] like the EGCG enhances 5-FU sensitivity and induces apoptosis in 5-FU resistant cancer cells [37].
		EGCG + NaB	10 μM E +(1,2,3,4,5 and 6 mM) N. IC50: 10 μM E + 5 mM N	The combination treatment induces apoptosis and G2/M cell cycle arrest through decrease in HDAC1, DNMT1, survivin and HDAC activity [43].
	CD133 and NANOG in HCT-116 stem cells	EGCG	10 and 20 μM	Inhibit sphere formation through inhibition of CD133, Nanog, ABCC1, ABCG2, Nek2, and p-Akt [174].
	CD44, CD133 and ALDH1 in HCT-116 stem cells	EGCG	50, 100, 200 and 400 μM	Induces apoptosis and cell cycle arrest, attenuate spheroid formation and enhance chemosensitivity of 5-FU in vivo [37].
	HCT-8	EGCG	10,20 and 35 μg/mL [182]	Inhibits proliferation in vitro and in vivo, induces apoptosis and affects cell cycle of cancer cells via inhibiting of HES1 and Notch2 expressions [182].
	Caco-2	EGCG	1, 5 and 10 μM [183]; 1, 10 and 50 μM [89]	Induces cell growth inhibition as EGCG and 67LR at a physiological concentration can activate myosin phosphatase by reducing MYPT1 phosphorylation [183] or through cyclin D1 degradation and p21 transcriptional activation via ERK, IKK and PI3K signaling pathway [89].
		EGCG (E) + Vitexin-2-O-xyloside (X) + Raphasatin (G)	E (10,20,30,40,50 μg/mL), X (30,50,80, 100,120 μg/mL) and G (5,10,15,30,50 μg/mL); IC50: E (135 ± 16), X (158 ± 13), G (36 ± 5) μg/mL	Mixture activates ROS mediated mitochondrial pathway causing G0/G1 cell cycle arrest and induces apoptosis [46].
		EGCG-CS-CPP-NPs	0.063, 0.125 and 0.250 mg/mL	Nanoparticles enhance stability, penetration and transportation of EGCG through cancer cells [184].
	HT-29	EGCG	0.1, 0.5, 1, 5 and 10 μM [120]; 1, 10 and 50 μM [89]; 10,20 and 35 μg/mL [182]; 5, 10 and 20 mg/kg/d oral gavage to male BALB nude mice for 28 days [185] or/14 days [182].	Inhibits Met signaling and helps to attenuate tumor spread/metastasis, independent of H2O2-related mechanisms [120]. Suppresses cancer cells growth through cyclin D1 degradation and p21 transcriptional activation via ERK, IKK and PI3K signaling pathway [89]. Inhibits proliferation in vitro and in vivo and induces apoptosis and affectes the cell cycle of cancer cells via inhibiting of HES1 and Notch2 expressions [182]. Inhibit tumor growth and metastasis in vivo by upregulating the Nrf2-UGT1A signaling [185].
		EGCG + NaB	10 μM E + (1,2,3,4,5 and 6 mM) N. IC50: 10 μM E + 5 mM N	The combination treatment induces apoptosis and G2/M cell cycle arrest through decrease in HDAC1, DNMT1, survivin and HDAC activity [43].
	SW837	EGCG	25 μg/mL in vitro; 0.01% and 0.1% in drinking water to BALB/c nude mice for 35 days [116]; 10,50 and 100 μM [186]	Inhibits tumor growth in vivo and in vitro through activation of VEGF/VEGFR axis via suppressing the expression of HIF-1α and several major growth factors [116]. Provides antitumor immunotherapy through inhibiting the expression and function of indoleamine 2,3–dioxygenase via suppression of STAT1 activation [186].
	SW480	EGCG	1, 10 and 50 μM [89]; 10,20 and 35 μg/mL [182]	Suppresses cancer cells growth through cyclin D1 degradation and p21 transcriptional activation via ERK, IKK and PI3K signaling pathway [89]. Inhibits proliferation in vitro and in vivo and induces apoptosis and affectes the cell cycle of cancer cells via inhibiting of HES1 and Notch2 expressions [182].
		EGCG + Panaxadiol	E (0,10,20 and 30 μM) and/or P (0,10 and 20 μM)	Inhibit cell proliferation and induce cell cycle arrest [35].
		EGCG + EPA-FFA + GS	EGCG (0–175 μM) + EPA-FFA (0–150 μM) + GS extract (0–15 μM) for 24 h	Combination completely inhibits the mTOR signaling and lead to changes in protein translation of ribosomal proteins, c-Myc and cyclin D1 and reduces clonal capability of cells, with block of cell cycle in G0/G1 and induction of apoptosis [128].
		EGCG + 5-FU	25–400 μM of EGCG and/or 2.5–40 μM 5-FU [37].	EGCG enhances 5-FU sensitivity and induces apoptosis in 5-FU resistant cancer cells [37]
	SW620	EGCG	25,50,75 and 100 μg/mL	Inhibits proliferation and migration in vitro through inactivation of PAR2-AP and factor VIIa and by the way inhibition of the ERK1/2 and NF-κB pathways [117].
	LoVo	EGCG	10,20 and 35 μg/mL	Inhibits proliferation in vitro and in vivo and induces apoptosis and affects the cell cycle of cancer cells via inhibiting of HES1 and Notch2 expressions [182].
		EGCG (E) + Vitexin-2-O-xyloside (X) + Raphasatin (G)	E (10,20,30,40,50 μg/mL), × (30,50,80, 100,120 μg/mL) and G (5,10,15,30,50 μg/mL); IC50: E (135 ± 16), X (158 ± 13), G (36 ± 5) μg/mL	Mixture activates ROS mediated mitochondrial pathway causing G0/G1 cell cycle arrest and induces apoptosis [46].
	RKO	EGCG	12.5,25,50 and 100 μM in vitro; 30 mg/kg IP injection to SCID male mice every other day for 2 weeks [118]	Inhibits cell proliferation and induces cell apoptosis through inhibition of Akt, activation and induction of p38 MAPK activation; inhibits liver metastasis in vivo and suppresses angiogenesis and induces apoptosis in liver metastasis [118].
		EGCG + NaB	10 μM E + (1,2,3,4,5 and 6 mM) N. IC50: 10 μM E + 5 mM N	The combination treatment induces apoptosis and G2/M cell cycle arrest through decrease in HDAC1, DNMT1, survivin and HDAC activity. Furthermore, p53-dependent induction of p21 and an increase in nuclear factor kappa B (NF-kB)-p65 [43].
	–	EGCG-(poly[lactic-co-glycolic acid])-NPs	–	Modify DNA damage in human lymphocytes from colon cancer patients and healthy individuals treated in vitro with platinum-based chemotherapeutic drugs [187].
Glioma	1321N1	EGCG	50,100,150,200,250 and 300 μg/mL; IC50: 82.0 ± 10.31 μg/mL (24 h)	Inhibits proliferation and induces apoptosis through activation of caspase-3 [30].
		EGCG + [6]-Gingerol	50 μg/mL EGCG + GING; IC50: 40 ± 8.62 μg/mL	Mixture inhibits proliferation and induces apoptosis through activation of caspase-3 [30].
		EGCG + Tocotrienol-rich fraction (TRF)	100 μg/mL EGCG + TRF; IC50: 100 ± 9.5 μg/mL
	LN18	EGCG	50,100,150,200,250 and 300 μg/mL; IC50: 134.0 ± 11.36 μg/mL (24 h)	Inhibits proliferation and induces apoptosis through activation of caspase-3 [30].
		EGCG + [6]-Gingerol	50 μg/mL EGCG + GING; IC50: 24 ± 2.65 μg/mL	Mixture inhibits proliferation and induces apoptosis through activation of caspase-3[30].
		EGCG + Tocotrienol-rich fraction (TRF)	80 μg/mL EGCG + TRF; IC50: 88 ± 11.14 μg/mL
	SW1783	EGCG	50,100,150,200,250 and 300 μg/mL; IC50: 300.0 ± 9.10 μg/mL (24 h)	Inhibits proliferation and induces apoptosis through activation of caspase-3 [30].
		EGCG + [6]-Gingerol	60 μg/mL EGCG + GING; IC50: 60 ± 5.6 μg/mL	Mixture inhibits proliferation and induces apoptosis through activation of caspase-3 [30].
		EGCG + Tocotrienol-rich fraction (TRF)	100 μg/mL EGCG + TRF; IC50: 270 ± 4.16 μg/mL
	U87	EGCG + Temozolomide	100 μM E + 100 μM TMZ	EGCG inhibits properties of glioma stem-like cells (CD133^high/ALDH1^high) and synergizes with TMZ through downregulation of P-glycoprotein inhibition [42].
	U251
	SHG-44
	C6
Skin cancer	A431	EGCG	5, 10, 20, 40, and 80 μg/mL [90];100–200 μM [91]; 10,20,40 and 60 μg/mL [188]	Inhibits cell growth, viability and induces cell apoptosis [90,91] through inhibition of EGFR signaling [91], inhibition of pRb-E2F/DP pathway [90], inducing cell cycle arrest [90,91] , inhibition of Cip1/p21 but no change in Kip1/27, CDK2, and cyclin D1 and a decrease in CDK4 only at low doses [91] and inactivation of β-catenin signaling [188].
	SCC-13	EGCG	10,20,40 and 60 μg/mL [188]; 10,20,40,60 and 100 μM [189]	Reduces cell viability [188], induces cell apoptosis [188,189] and inhibits cell growth [189] through inactivation of β-catenin signaling [188] and influencing PcG-mediated epigenetic regulation of cell cycle-related genes [189].
	–	Green tea polyphenols	200μL of a 5% solution	Prevent the adverse effects of UV radiation in humans [190].
Esophageal cancer	TE-8	EGCG	40 μM in vitro	Reduces cell viability and invasion in vitro through reduction of p-ERK1/2, c-Jun and COX-2, and activation of caspase-3 whereas it inhibits tumor growth in vivo through suppressing the expression of Ki67, p-ERK1/2 and COX-2 [32].
		EGCG (E) + Curcumin (C)	E (40 μmol/L), C (40 μmol/L), and L (4 μmol/L) in vitro
		EGCG (E) + Curcumin (C) + Lovastatin (L)
	SKGT-4	EGCG	40 μM in vitro and 50 μg/kg/d by oral intake into nude mice for 30 days (5 day/week)
		EGCG (E) + Curcumin (C)	E (40 μmol/L), C (40 μmol/L), and L (4 μmol/L) in vitro
		EGCG (E) + Curcumin (C) + Lovastatin (L)
Adrenal cancer	NCI-H295	EGCG	10, 20, 30 and 40 µM in vitro; IC50: 20.34 µM (48 h)	Induces cell apoptosis through activation of caspase-dependent, caspase-independent, the mitochondrial, death receptor and endoplasmic reticulum stress apoptotic signaling pathways. EGCG also downregulate the expression of anti-apoptotic proteins, including BCL-2, BCL-XL and XIAP. It upregulate the expression of pro-apoptotic proteins, including Apaf-1, BAD and BAX. It regulate molecular chaperones, such as 70 kDa heat shock protein (HSP70), HSP90 and GRP78 [76].
Bladder cancer	T-24	EGCG	10, 20, 40, 80 µg/mL	Inhibit cell adhesion, migration and invasion through downregulion of MMP-9 expression via blocking of NF-κB signaling pathway [121].
		EGCG (in green tea extract) + Ascorbic acid + Lysine + Proline + Arginine	10,50,100,500 and 1000 µg/mL of the mixture	Mixture inhibits critical steps of cancer development and spread, such as MMP-2 and -9 secretions and invasion [137].
Pheochromocytoma	PC-12	EGCG	15 mg/kg IP injection into male BALB/c nude mice every other day for 15 days	Inhibits tumor growth and induces cancer cell apoptosis via acetylation of amyloid precursor protein [77].
Neuroblastoma	(Nanog^high/Oct4^high/ATP7A^low/DKK2^low)in BE(2)-C CSCs	EGCG	1,10,50 and 100 μM	Inhibits the development of TICs in BE(2)-C cells as well as inhibits sphere formation and induces apoptosis [134].
Ehrlich’s ascites carcinoma	EAC	EGCG + HDHA-DOX-NPs	E (20 mg/kg b.wt., orally through gavage) + HDHA-DOX-NPs (1.5 mg/kg b.wt.) intravenously into Swiss albino mice.	EGCG enhances the anticancer activities of HDHA-NPs significantly increasing the mean survival time of the animals and inducing apoptosis [145].
Head and neck squamous carcinoma (HNSC) CSCs	K3	EGCG + Cisplatin	5,10,20 and 50 μM E and/or 5,10 and 20 μM C	Inhibit sphere formation and CD44^+ cell population; enhances chemosensitivity of cisplatin in vitro and in vivo through downregulation of Oct4, Sox2, ABCC2, ABCG2 and Notch1 [39].
	K4
	K5

Fig. 5 Schematic drawing of the regulative actions of EGCG combined with nanoparticles. This carton is based on the available literature.

A.A.RahmanS.MakpolR.JamalR.HarunN.MokhtarW.Z.NgahTocotrienol-rich fraction, [6]-gingerol and epigallocatechin gallate inhibit proliferation and induce apoptosis of glioma cancer cellsMolecules1920141452814541

 PubMed Web of Science ®Google Scholar

M.W.RoomiV.IvanovT.KalinovskyA.NiedzwieckiM.RathAnti-tumor effect of ascorbic acid, lysine, proline, arginine, and epigallocatechin gallate on prostate cancer cell lines PC-3, LNCaP, and DU145Res Commun Mol Pathol Pharmacol115–1162004251264

 PubMedGoogle Scholar

M.W.RoomiV.IvanovT.KalinovskyA.NiedzwieckiM.RathAntitumor effect of ascorbic acid, lysine, proline, arginine, and green tea extract on bladder cancer cell line T-24Int J Urol132006415419

 Web of Science ®Google Scholar

T.J.Somers-EdgarM.J.ScandlynE.C.StuartM.J.Le NedelecS.P.ValentineR.J.RosengrenThe combination of epigallocatechin gallate and curcumin suppresses ER alpha-breast cancer cell growth in vitro and in vivoInt J Cancer122200819661971

 PubMed Web of Science ®Google Scholar

S.WangR.ChenZ.ZhongZ.ShiM.ChenY.WangEpigallocatechin-3-gallate potentiates the effect of curcumin in inducing growth inhibition and apoptosis of resistant breast cancer cellsAm J Chin Med42201412791300

 PubMed Web of Science ®Google Scholar

E.RanzatoV.MagnelliS.MartinottiZ.WaheedS.M.CainT.P.Snutchet al.Epigallocatechin-3-gallate elicits Ca2+ spike in MCF-7 breast cancer cells: essential role of Cav3.2 channelsCell Calcium562014285295

 PubMed Web of Science ®Google Scholar

D.H.ZhouX.WangM.YangX.ShiW.HuangQ.FengCombination of low concentration of (-)-epigallocatechin gallate (EGCG) and curcumin strongly suppresses the growth of non-small cell lung cancer in vitro and in vivo through causing cell cycle arrestInt J Mol Sci1420131202312036

 PubMed Web of Science ®Google Scholar

P.WangD.HeberS.M.HenningQuercetin increased the antiproliferative activity of green tea polyphenol (-)-epigallocatechin gallate in prostate cancer cellsNutr Cancer642012580587

 PubMed Web of Science ®Google Scholar

F.YeG.H.ZhangB.X.GuanX.C.XuSuppression of esophageal cancer cell growth using curcumin, (-)-epigallocatechin-3-gallate and lovastatinWorld J Gastroenterol182012126135

 PubMed Web of Science ®Google Scholar

S.GuptaN.AhmadR.R.MohanM.M.HusainH.MukhtarProstate cancer chemoprevention by green tea: in vitro and in vivo inhibition of testosterone-mediated induction of ornithine decarboxylaseCancer Res59199921152120

 PubMed Web of Science ®Google Scholar

L.D'AngeloG.PiazziA.PacilliA.ProssomaritiC.FazioL.Montanaroet al.A combination of eicosapentaenoic acid-free fatty acid, epigallocatechin-3-gallate and proanthocyanidins has a strong effect on mTOR signaling in colorectal cancer cellsCarcinogenesis35201423142320

 PubMed Web of Science ®Google Scholar

H.FuJ.HeF.MeiQ.ZhangY.HaraS.Ryotaet al.Lung cancer inhibitory effect of epigallocatechin-3-gallate is dependent on its presence in a complex mixture (polyphenon E)Cancer Prev Res (Phila)22009531537

 PubMed Web of Science ®Google Scholar

S.F.KostinD.E.McDonaldD.W.McFaddenInhibitory effects of (-)-epigallocatechin-3-gallate and pterostilbene on pancreatic cancer growth in vitroJ Surg Res1772012255262

 PubMed Web of Science ®Google Scholar

S.NairA.BarveT.O.KhorG.X.ShenW.LinJ.Y.Chanet al.Regulation of Nrf2- and AP-1-mediated gene expression by epigallocatechin-3-gallate and sulforaphane in prostate of Nrf2-knockout or C57BL/6J mice and PC-3 AP-1 human prostate cancer cellsActa Pharmacol Sin31201012231240

 PubMed Web of Science ®Google Scholar

A.BasuS.HaldarCombinatorial effect of epigallocatechin-3-gallate and TRAIL on pancreatic cancer cell deathInt J Oncol342009281286

 PubMed Web of Science ®Google Scholar

J.KimX.ZhangK.M.Rieger-ChristI.C.SummerhayesD.E.WazerK.E.Paulsonet al.Suppression of Wnt signaling by the green tea compound (-)-epigallocatechin 3-gallate (EGCG) in invasive breast cancer cells. Requirement of the transcriptional repressor HBP1J Biol Chem28120061086510875

 PubMed Web of Science ®Google Scholar

R.L.ThangapazhamN.PassiR.K.MaheshwariGreen tea polyphenol and epigallocatechin gallate induce apoptosis and inhibit invasion in human breast cancer cellsCancer Biol Ther6200719381943

 PubMed Web of Science ®Google Scholar

S.M.MeeranS.N.PatelT.H.ChanT.O.TollefsbolA novel prodrug of epigallocatechin-3-gallate: differential epigenetic hTERT repression in human breast cancer cellsCancer Prev Res (Phila)4201112431254

 PubMed Web of Science ®Google Scholar

T.SenA.ChatterjeeEpigallocatechin-3-gallate (EGCG) downregulates EGF-induced MMP-9 in breast cancer cells: involvement of integrin receptor alpha5beta1 in the processEur J Nutr502011465478

 PubMed Web of Science ®Google Scholar

L.MoreiraI.AraujoT.CostaA.Correia-BrancoA.Fariaet al.Quercetin and epigallocatechin gallate inhibit glucose uptake and metabolism by breast cancer cells by an estrogen receptor-independent mechanismExp Cell Res319201317841795

 PubMed Web of Science ®Google Scholar

K.R.Landis-PiwowarC.D.HuoD.ChenV.MilacicG.Q.ShiT.H.Chanet al.A novel prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate as a potential anticancer agentCancer Research67200743034310

 PubMed Web of Science ®Google Scholar

A.PapiF.FarabegoliR.IoriM.OrlandiG.R.De NicolaM.Bagattaet al.Vitexin-2-O-xyloside, raphasatin and (-)-epigallocatechin-3-gallate synergistically affect cell growth and apoptosis of colon cancer cellsFood Chem138201315211530

 PubMed Web of Science ®Google Scholar

S.NarayananU.MonyD.K.VijaykumarM.KoyakuttyB.Paul-PrasanthD.MenonSequential release of epigallocatechin gallate and paclitaxel from PLGA-casein core/shell nanoparticles sensitizes drug-resistant breast cancer cellsNanomedicine11201513991406

 PubMed Web of Science ®Google Scholar

T.G.ShutavaS.S.BalkundiP.VangalaJ.J.SteffanR.L.BigelowJ.A.Cardelliet al.Layer-by-layer-coated gelatin nanoparticles as a vehicle for delivery of natural polyphenolsACS Nano3200918771885

 PubMed Web of Science ®Google Scholar

I.A.SiddiquiV.M.AdhamiN.AhmadH.MukhtarNanochemoprevention: sustained release of bioactive food components for cancer preventionNutr Cancer622010883890

 PubMed Web of Science ®Google Scholar

Y.TangD.Y.ZhaoS.ElliottW.ZhaoT.J.CurielB.S.Beckmanet al.Epigallocatechin-3 gallate induces growth inhibition and apoptosis in human breast cancer cells through survivin suppressionInt J Oncol312007705711

 PubMed Web of Science ®Google Scholar

Y.ZhangG.HanB.FanY.ZhouX.ZhouL.Weiet al.Green tea (-)-epigallocatechin-3-gallate down-regulates VASP expression and inhibits breast cancer cell migration and invasion by attenuating Rac1 activityEur J Pharmacol6062009172179

 PubMed Web of Science ®Google Scholar

S.H.TuC.Y.KuC.T.HoC.S.ChenC.S.HuangC.H.Leeet al.Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced alpha9-nicotinic acetylcholine receptor upregulation in human breast cancer cellsMol Nutr Food Res552011455466

 PubMed Web of Science ®Google Scholar

F.De AmicisA.RussoP.AvenaM.SantoroA.VivacquaD.Bonofiglioet al.In vitro mechanism for downregulation of ER-alpha expression by epigallocatechin gallate in ER+/PR+ human breast cancer cellsMol Nutr Food Res572013840853

 PubMed Web of Science ®Google Scholar

C.BraicuC.D.GhermanA.IrimieI.Berindan-NeagoeEpigallocatechin-3-Gallate (EGCG) inhibits cell proliferation and migratory behaviour of triple negative breast cancer cellsJ Nanosci Nanotechnol132013632637

 PubMed Web of Science ®Google Scholar

S.PianettiS.GuoK.T.KavanaghG.E.SonensheinGreen tea polyphenol epigallocatechin-3 gallate inhibits Her-2/neu signaling, proliferation, and transformed phenotype of breast cancer cellsCancer Res622002652655

 PubMed Web of Science ®Google Scholar

K.BelguiseS.GuoG.E.SonensheinActivation of FOXO3a by the green tea polyphenol epigallocatechin-3-gallate induces estrogen receptor alpha expression reversing invasive phenotype of breast cancer cellsCancer Res67200757635770

 PubMed Web of Science ®Google Scholar

J.Y.JangJ.K.LeeY.K.JeonC.W.KimExosome derived from epigallocatechin gallate treated breast cancer cells suppresses tumor growth by inhibiting tumor-associated macrophage infiltration and M2 polarizationBMC Cancer132013421

 PubMed Web of Science ®Google Scholar

N.D.MinevaK.E.PaulsonS.P.NaberA.S.YeeG.E.SonensheinEpigallocatechin-3-gallate inhibits stem-like inflammatory breast cancer cellsPLoS One82013e73464

 PubMed Web of Science ®Google Scholar

X.PanB.ZhaoZ.SongS.HanM.WangEstrogen receptor-alpha36 is involved in epigallocatechin-3-gallate induced growth inhibition of ER-negative breast cancer stem/progenitor cellsJ Pharmacol Sci13020168593

 PubMed Web of Science ®Google Scholar

J.RelatA.BlancafortG.OliverasS.CufiD.HaroP.F.Marreroet al.Different fatty acid metabolism effects of (-)-epigallocatechin-3-gallate and C75 in adenocarcinoma lung cancerBMC Cancer122012280

 PubMed Web of Science ®Google Scholar

Y.SakamotoN.TerashitaT.MuraguchiT.FukusatoS.KubotaEffects of epigallocatechin-3-gallate (EGCG) on A549 lung cancer tumor growth and angiogenesisBiosci Biotechnol Biochem77201317991803

 PubMed Web of Science ®Google Scholar

L.JinC.LiY.XuL.WangJ.LiuD.Wanget al.Epigallocatechin gallate promotes p53 accumulation and activity via the inhibition of MDM2-mediated p53 ubiquitination in human lung cancer cellsOncol Rep29201319831990

 PubMed Web of Science ®Google Scholar

L.HeE.ZhangJ.ShiX.LiK.ZhouQ.Zhanget al.(-)-Epigallocatechin-3-gallate inhibits human papillomavirus (HPV)-16 oncoprotein-induced angiogenesis in non-small cell lung cancer cells by targeting HIF-1alphaCancer Chemother Pharmacol712013713725

 PubMed Web of Science ®Google Scholar

J.ShiF.LiuW.ZhangX.LiuB.LinX.TangEpigallocatechin-3-gallate inhibits nicotine-induced migration and invasion by the suppression of angiogenesis and epithelial-mesenchymal transition in non-small cell lung cancer cellsOncol Rep33201529722980

 PubMed Web of Science ®Google Scholar

Y.C.MaC.LiF.GaoY.XuZ.B.JiangJ.X.Liuet al.Epigallocatechin gallate inhibits the growth of human lung cancer by directly targeting the EGFR signaling pathwayOncol Rep31201413431349

 PubMed Web of Science ®Google Scholar

K.C.KimC.LeeReversal of Cisplatin resistance by epigallocatechin gallate is mediated by downregulation of axl and tyro 3 expression in human lung cancer cellsKorean J Physiol Pharmacol1820146166

 PubMed Web of Science ®Google Scholar

J.I.SonodaR.IkedaY.BabaK.NarumiA.KawachiE.Tomishigeet al.Green tea catechin, epigallocatechin-3-gallate, attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expressionExp Ther Med820145963

 PubMed Web of Science ®Google Scholar

X.LiY.FengJ.LiuX.FengK.ZhouX.TangEpigallocatechin-3-gallate inhibits IGF-I-stimulated lung cancer angiogenesis through downregulation of HIF-1alpha and VEGF expressionJ Nutrigenet Nutrigenomics62013169178

 PubMed Web of Science ®Google Scholar

H.WangS.BianC.S.YangGreen tea polyphenol EGCG suppresses lung cancer cell growth through upregulating miR-210 expression caused by stabilizing HIF-1alphaCarcinogenesis32201118811889

 PubMed Web of Science ®Google Scholar

J.D.LambertS.SangC.S.YangN-Acetylcysteine enhances the lung cancer inhibitory effect of epigallocatechin-3-gallate and forms a new adductFree Radic Biol Med44200810691074

 PubMed Web of Science ®Google Scholar

G.X.LiY.K.ChenZ.HouH.XiaoH.JinG.Luet al.Pro-oxidative activities and dose-response relationship of (-)-epigallocatechin-3-gallate in the inhibition of lung cancer cell growth: a comparative study in vivo and in vitroCarcinogenesis312010902910

 PubMed Web of Science ®Google Scholar

A.TakahashiT.WatanabeA.MondalK.SuzukiM.Kurusu-KannoZ.Liet al.Mechanism-based inhibition of cancer metastasis with (-)-epigallocatechin gallateBiochem Biophys Res Commun443201416

 PubMed Web of Science ®Google Scholar

D.SadavaE.WhitlockS.E.KaneThe green tea polyphenol, epigallocatechin-3-gallate inhibits telomerase and induces apoptosis in drug-resistant lung cancer cellsBiochem Biophys Res Commun3602007233237

 PubMed Web of Science ®Google Scholar

S.ShankarG.SuthakarR.K.SrivastavaEpigallocatechin-3-gallate inhibits cell cycle and induces apoptosis in pancreatic cancerFront Biosci12200750395051

 PubMed Web of Science ®Google Scholar

Y.LiT.ZhangY.JiangH.F.LeeS.J.SchwartzD.Sun(-)-Epigallocatechin-3-gallate inhibits Hsp90 function by impairing Hsp90 association with cochaperones in pancreatic cancer cell line Mia Paca-2Mol Pharm6200911521159

 PubMed Web of Science ®Google Scholar

S.D.RaoK.PagidasEpigallocatechin-3-gallate, a natural polyphenol, inhibits cell proliferation and induces apoptosis in human ovarian cancer cellsAnticancer Res30201025192523

 PubMed Web of Science ®Google Scholar

C.YanJ.YangL.ShenX.ChenInhibitory effect of Epigallocatechin gallate on ovarian cancer cell proliferation associated with aquaporin 5 expressionArch Gynecol Obstet2852012459467

 PubMed Web of Science ®Google Scholar

Z.YinE.C.HenryT.A.Gasiewicz(-)-Epigallocatechin-3-gallate is a novel Hsp90 inhibitorBiochemistry482009336345

 PubMed Web of Science ®Google Scholar

C.W.ChengP.C.ShiehY.C.LinY.J.ChenY.H.LinD.H.Kuoet al.Indoleamine 2,3-dioxygenase, an immunomodulatory protein, is suppressed by (-)-epigallocatechin-3-gallate via blocking of gamma-interferon-induced JAK-PKC-delta-STAT1 signaling in human oral cancer cellsJ Agric Food Chem582010887894

 PubMed Web of Science ®Google Scholar

P.N.ChenS.C.ChuW.H.KuoM.Y.ChouJ.K.LinY.S.HsiehEpigallocatechin-3 gallate inhibits invasion, epithelial-mesenchymal transition, and tumor growth in oral cancer cellsJ Agric Food Chem59201138363844

 PubMed Web of Science ®Google Scholar

A.I.IrimieC.BraicuO.ZanoagaV.PileczkiC.GhermanI.Berindan-Neagoeet al.Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis and autophagy in oral cancer SSC-4 cellsOnco Targets Ther82015461470

 PubMed Web of Science ®Google Scholar

Y.W.KohE.C.ChoiS.U.KangH.S.HwangM.H.LeeJ.Pyunet al.Green tea (-)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-MetJ Nutr Biochem22201110741083

 PubMed Web of Science ®Google Scholar

Y.S.HwangK.K.ParkW.Y.ChungEpigallocatechin-3 gallate inhibits cancer invasion by repressing functional invadopodia formation in oral squamous cell carcinomaEur J Pharmacol7152013286295

 PubMed Web of Science ®Google Scholar

C.H.LinL.K.ChaoP.H.HungY.J.ChenEGCG inhibits the growth and tumorigenicity of nasopharyngeal tumor-initiating cells through attenuation of STAT3 activationInt J Clin Exp Pathol7201423722381

 PubMed Web of Science ®Google Scholar

Y.J.LiS.L.WuS.M.LuF.ChenY.GuoS.M.Ganet al.(-)-Epigallocatechin-3-gallate inhibits nasopharyngeal cancer stem cell self-renewal and migration and reverses the epithelial-mesenchymal transition via NF-kappaB p65 inactivationTumour Biol36201527472761

 PubMed Web of Science ®Google Scholar

H.WuY.XinY.XiaoJ.ZhaoLow-dose docetaxel combined with (-)-epigallocatechin-3-gallate inhibits angiogenesis and tumor growth in nude mice with gastric cancer xenograftsCancer Biother Radiopharm272012204209

 PubMed Web of Science ®Google Scholar

H.WuY.XinC.XuY.XiaoCapecitabine combined with (-)-epigallocatechin-3-gallate inhibits angiogenesis and tumor growth in nude mice with gastric cancer xenograftsExp Ther Med32012650654

 PubMed Web of Science ®Google Scholar

B.H.ZhuH.Y.ChenW.H.ZhanC.Y.WangS.R.CaiZ.Wanget al.(-)-Epigallocatechin-3-gallate inhibits VEGF expression induced by IL-6 via Stat3 in gastric cancerWorld J Gastroenterol17201123152325

 PubMed Web of Science ®Google Scholar

J.MaM.ShiG.LiN.WangJ.WeiT.Wanget al.Regulation of Id1 expression by epigallocatechin3gallate and its effect on the proliferation and apoptosis of poorly differentiated AGS gastric cancer cellsInt J Oncol43201310521058

 PubMed Web of Science ®Google Scholar

T.TanakaT.IshiiD.MizunoT.MoriR.YamajiY.Nakamuraet al.(-)-Epigallocatechin-3-gallate suppresses growth of AZ521 human gastric cancer cells by targeting the DEAD-box RNA helicase p68Free Radic Biol Med50201113241335

 PubMed Web of Science ®Google Scholar

C.OnodaK.KuribayashiS.NirasawaN.TsujiM.TanakaD.Kobayashiet al.(-)-Epigallocatechin-3-gallate induces apoptosis in gastric cancer cell lines by down-regulating survivin expressionInt J Oncol38201114031408

 PubMed Web of Science ®Google Scholar

B.H.ZhuW.H.ZhanZ.R.LiZ.WangY.L.HeJ.S.Penget al.(-)-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesisWorld J Gastroenterol13200711621169

 PubMed Web of Science ®Google Scholar

D.Z.WeiJ.Y.YangJ.W.LiuW.Y.TongInhibition of liver cancer cell proliferation and migration by a combination of (-)-epigallocatechin-3-gallate and ascorbic acidJ Chemother152003591595

 PubMed Web of Science ®Google Scholar

Y.ZhangN.D.YangF.ZhouT.ShenT.DuanJ.Zhouet al.(-)-Epigallocatechin-3-gallate induces non-apoptotic cell death in human cancer cells via ROS-mediated lysosomal membrane permeabilizationPLoS One72012e46749

 PubMed Web of Science ®Google Scholar

G.Y.WubetuM.ShimadaY.MorineT.IkemotoD.IshikawaS.Iwahashiet al.Epigallocatechin gallate hinders human hepatoma and colon cancer sphere formationJ Gastroenterol Hepatol312016256264

 PubMed Web of Science ®Google Scholar

D.S.AlbrechtE.A.ClubbsM.FerruzziJ.A.BomserEpigallocatechin-3-gallate (EGCG) inhibits PC-3 prostate cancer cell proliferation via MEK-independent ERK1/2 activationChem Biol Interact17120088995

 PubMed Web of Science ®Google Scholar

R.M.HagenV.S.ChedeaC.P.MintoffE.BowlerH.R.MorseM.R.LadomeryEpigallocatechin-3-gallate promotes apoptosis and expression of the caspase 9a splice variant in PC3 prostate cancer cellsInt J Oncol432013194200

 PubMed Web of Science ®Google Scholar

D.W.EomJ.H.LeeY.J.KimG.S.HwangS.N.KimJ.H.Kwaket al.Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cellsBMB Rep482015461466

 PubMed Web of Science ®Google Scholar

R.ShuklaN.ChandaA.ZambreA.UpendranK.KattiR.R.Kulkarniet al.Laminin receptor specific therapeutic gold nanoparticles (198AuNP-EGCg) show efficacy in treating prostate cancerProc Natl Acad Sci U S A10920121242612431

 PubMed Web of Science ®Google Scholar

S.S.ShafieiM.Solati-HashjinA.SamadikuchaksaraeiR.KalantarinejadM.Asadi-EydivandN.A.Abu Osmanpigallocatechin gallate/layered double hydroxide nanohybrids: preparation, characterization, and in vitro anti-tumor studyPLoS One102015e0136530

 PubMed Web of Science ®Google Scholar

I.A.SiddiquiV.M.AdhamiD.J.BharaliB.B.HafeezM.AsimS.I.Khwajaet al.Introducing nanochemoprevention as a novel approach for cancer control: proof of principle with green tea polyphenol epigallocatechin-3-gallateCancer Res69200917121716

 PubMed Web of Science ®Google Scholar

V.SannaC.K.SinghR.JashariV.M.AdhamiJ.C.ChamcheuI.Radyet al.Targeted nanoparticles encapsulating (-)-epigallocatechin-3-gallate for prostate cancer prevention and therapySci Rep7201741573

 PubMed Web of Science ®Google Scholar

M.E.StearnsM.D.AmatangeloD.VarmaC.SellS.M.GoodyearCombination therapy with epigallocatechin-3-gallate and doxorubicin in human prostate tumor modeling studies: inhibition of metastatic tumor growth in severe combined immunodeficiency miceAm J Pathol177201031693179

 PubMed Web of Science ®Google Scholar

S.N.TangC.SinghD.NallD.MeekerS.ShankarR.K.SrivastavaThe dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transitionJ Mol Signal5201014

 PubMedGoogle Scholar

S.I.WangH.MukhtarGene expression profile in human prostate LNCaP cancer cells by (-) epigallocatechin-3-gallateCancer Lett18220024351

 PubMed Web of Science ®Google Scholar

C.P.ChuuR.Y.ChenJ.M.KokontisR.A.HiipakkaS.LiaoSuppression of androgen receptor signaling and prostate specific antigen expression by (-)-epigallocatechin-3-gallate in different progression stages of LNCaP prostate cancer cellsCancer Lett27520098692

 PubMed Web of Science ®Google Scholar

S.GuptaN.AhmadA.L.NieminenH.MukhtarGrowth inhibition, cell-cycle dysregulation, and induction of apoptosis by green tea constituent (-)-epigallocatechin-3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cellsToxicol Appl Pharmacol16420008290

 PubMed Web of Science ®Google Scholar

D.DuhonR.L.BigelowD.T.ColemanJ.J.SteffanC.YuW.Langstonet al.The polyphenol epigallocatechin-3-gallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cellsMol Carcinog492010739749

 PubMed Web of Science ®Google Scholar

S.C.LeeW.K.ChanT.W.LeeW.H.LamX.WangT.H.Chanet al.Effect of a prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate on the growth of androgen-independent prostate cancer in vivoNutr Cancer602008483491

 PubMed Web of Science ®Google Scholar

M.A.MosesE.C.HenryW.A.RickeT.A.GasiewiczThe heat shock protein 90 inhibitor, (-)-epigallocatechin gallate, has anticancer activity in a novel human prostate cancer progression modelCancer Prev Res (Phila)82015249257

 PubMed Web of Science ®Google Scholar

N.KhanD.J.BharaliV.M.AdhamiI.A.SiddiquiH.CuiS.M.Shabanaet al.Oral administration of naturally occurring chitosan-based nanoformulated green tea polyphenol EGCG effectively inhibits prostate cancer cell growth in a xenograft modelCarcinogenesis352014415423

 PubMed Web of Science ®Google Scholar

C.E.HarperB.B.PatelJ.WangI.A.EltoumC.A.LamartiniereEpigallocatechin-3-Gallate suppresses early stage, but not late stage prostate cancer in TRAMP mice: mechanisms of actionProstate67200715761589

 PubMed Web of Science ®Google Scholar

S.GuptaK.HastakN.AhmadJ.S.LewinH.MukhtarInhibition of prostate carcinogenesis in TRAMP mice by oral infusion of green tea polyphenolsProc Natl Acad Sci U S A9820011035010355

 PubMed Web of Science ®Google Scholar

I.A.SiddiquiD.J.BharaliM.NihalV.M.AdhamiN.KhanJ.C.Chamcheuet al.Excellent anti-proliferative and pro-apoptotic effects of (-)-epigallocatechin-3-gallate encapsulated in chitosan nanoparticles on human melanoma cell growth both in vitro and in vivoNanomedicine10201416191626

 PubMed Web of Science ®Google Scholar

J.LiS.WuC.WuL.QiuG.ZhuC.Cuiet al.Versatile surface engineering of porous nanomaterials with bioinspired polyphenol coatings for targeted and controlled drug deliveryNanoscale8201686008606

 Web of Science ®Google Scholar

Y.QiaoJ.CaoL.XieX.ShiCell growth inhibition and gene expression regulation by (-)-epigallocatechin-3-gallate in human cervical cancer cellsArch Pharm Res32200913091315

 PubMed Web of Science ®Google Scholar

C.SharmaA.Nusri QelS.BegumE.JavedT.A.RizviA.Hussain(-)-Epigallocatechin-3-gallate induces apoptosis and inhibits invasion and migration of human cervical cancer cellsAsian Pac J Cancer Prev13201248154822

 PubMedGoogle Scholar

C.A.LarsenR.H.Dashwood(-)-Epigallocatechin-3-gallate inhibits Met signaling, proliferation, and invasiveness in human colon cancer cellsArch Biochem Biophys50120105257

 PubMed Web of Science ®Google Scholar

C.A.LarsenR.H.DashwoodSuppression of Met activation in human colon cancer cells treated with (-)-epigallocatechin-3-gallate: minor role of hydrogen peroxideBiochem Biophys Res Commun3892009527530

 PubMed Web of Science ®Google Scholar

X.ZhangK.W.MinJ.WimalasenaS.J.BaekCyclin D1 degradation and p21 induction contribute to growth inhibition of colorectal cancer cells induced by epigallocatechin-3-gallateJ Cancer Res Clin Oncol138201220512060

 PubMed Web of Science ®Google Scholar

N.Y.MinJ.H.KimJ.H.ChoiW.LiangY.J.KoS.Rheeet al.Selective death of cancer cells by preferential induction of reactive oxygen species in response to (-)-epigallocatechin-3-gallateBiochem Biophys Res Commun42120129197

 PubMed Web of Science ®Google Scholar

T.MaruyamaS.MurataK.NakayamaN.SanoK.OgawaT.Nowatariet al.(-)-Epigallocatechin-3-gallate suppresses liver metastasis of human colorectal cancerOncol Rep312014625633

 PubMed Web of Science ®Google Scholar

G.J.DuC.Z.WangL.W.QiZ.Y.ZhangT.CalwayT.C.Heet al.The synergistic apoptotic interaction of panaxadiol and epigallocatechin gallate in human colorectal cancer cellsPhytother Res272013272277

 PubMed Web of Science ®Google Scholar

S.TodenH.M.TranO.A.Tovar-CamargoY.OkugawaA.GoelEpigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancerOncotarget720161615816171

 PubMed Web of Science ®Google Scholar

S.N.SaldanhaR.KalaT.O.TollefsbolMolecular mechanisms for inhibition of colon cancer cells by combined epigenetic-modulating epigallocatechin gallate and sodium butyrateExp Cell Res32420144053

 PubMed Web of Science ®Google Scholar

H.JinW.GongC.ZhangS.WangEpigallocatechin gallate inhibits the proliferation of colorectal cancer cells by regulating Notch signalingOnco Targets Ther62013145153

 PubMed Web of Science ®Google Scholar

D.UmedaS.YanoK.YamadaH.TachibanaInvolvement of 67-kDa laminin receptor-mediated myosin phosphatase activation in antiproliferative effect of epigallocatechin-3-O-gallate at a physiological concentration on Caco-2 colon cancer cellsBiochem Biophys Res Commun3712008172176

 PubMed Web of Science ®Google Scholar

B.HuY.TingX.YangW.TangX.ZengQ.HuangNanochemoprevention by encapsulation of (-)-epigallocatechin-3-gallate with bioactive peptides/chitosan nanoparticles for enhancement of its bioavailabilityChem Commun (Camb)48201224212423

 PubMed Web of Science ®Google Scholar

J.H.YuanY.Q.LiX.Y.YangInhibition of epigallocatechin gallate on orthotopic colon cancer by upregulating the Nrf2-UGT1A signal pathway in nude micePharmacology802007269278

 PubMed Web of Science ®Google Scholar

M.ShimizuY.ShirakamiH.SakaiY.YasudaM.KubotaS.Adachiet al.(-)-Epigallocatechin gallate inhibits growth and activation of the VEGF/VEGFR axis in human colorectal cancer cellsChem Biol Interact1852010247252

 PubMed Web of Science ®Google Scholar

K.OgawaT.HaraM.ShimizuJ.NaganoT.OhnoM.Hoshiet al.(-)-Epigallocatechin gallate inhibits the expression of indoleamine 2,3-dioxygenase in human colorectal cancer cellsOncol Lett42012546550

 PubMed Web of Science ®Google Scholar

F.ZhouH.ZhouT.WangY.MuB.WuD.L.Guoet al.Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitroActa Pharmacol Sin332012120126

 PubMed Web of Science ®Google Scholar

A.AlotaibiP.BhatnagarM.NajafzadehK.C.GuptaD.AndersonTea phenols in bulk and nanoparticle form modify DNA damage in human lymphocytes from colon cancer patients and healthy individuals treated in vitro with platinum-based chemotherapeutic drugsNanomedicine (Lond)82013389401

 Web of Science ®Google Scholar

Y.ZhangS.X.WangJ.W.MaH.Y.LiJ.C.YeS.M.Xieet al.EGCG inhibits properties of glioma stem-like cells and synergizes with temozolomide through downregulation of P-glycoprotein inhibitionJ Neurooncol12120154152

 PubMed Web of Science ®Google Scholar

N.AhmadV.M.AdhamiS.GuptaP.ChengH.MukhtarRole of the retinoblastoma (pRb)-E2F/DP pathway in cancer chemopreventive effects of green tea polyphenol epigallocatechin-3-gallateArch Biochem Biophys3982002125131

 PubMed Web of Science ®Google Scholar

N.BhatiaC.AgarwalR.AgarwalDifferential responses of skin cancer-chemopreventive agents silibinin, quercetin, and epigallocatechin 3-gallate on mitogenic signaling and cell cycle regulators in human epidermoid carcinoma A431 cellsNutr Cancer392001292299

 PubMed Web of Science ®Google Scholar

T.SinghS.K.KatiyarGreen tea polyphenol, (-)-epigallocatechin-3-gallate, induces toxicity in human skin cancer cells by targeting beta-catenin signalingToxicol Appl Pharmacol2732013418424

 PubMed Web of Science ®Google Scholar

S.BalasubramanianG.AdhikaryR.L.EckertThe Bmi-1 polycomb protein antagonizes the (-)-epigallocatechin-3-gallate-dependent suppression of skin cancer cell survivalCarcinogenesis312010496503

 PubMed Web of Science ®Google Scholar

H.MukhtarM.S.MatsuiD.MaesK.MarenusK.TubesingC.A.ElmetsPrevention by green tea polyphenols against ultraviolet-induced erythema in humansJ Invest Dermatol1061996243

 Web of Science ®Google Scholar

P.P.WuS.C.KuoW.W.HuangJ.S.YangK.C.LaiH.J.Chenet al.(-)-Epigallocatechin gallate induced apoptosis in human adrenal cancer NCI-H295 cells through caspase-dependent and caspase-independent pathwayAnticancer Res29200914351442

 PubMed Web of Science ®Google Scholar

J.QinY.WangY.BaiK.YangQ.MaoY.Linet al.Epigallocatechin-3-gallate inhibits bladder cancer cell invasion via suppression of NF-kappaBmediated matrix metalloproteinase-9 expressionMol Med Rep6201210401044

 PubMed Web of Science ®Google Scholar

Q.HuX.ChangR.YanC.RongC.YangS.Chenget al.(-)-Epigallocatechin-3-gallate induces cancer cell apoptosis via acetylation of amyloid precursor proteinMed Oncol322015390

 PubMed Web of Science ®Google Scholar

N.NishimuraT.B.HartomoT.V.PhamM.J.LeeT.YamamotoS.Morikawaet al.Y.TakeshimaK.IijimaM.MatsuoH.NishioEpigallocatechin gallate inhibits sphere formation of neuroblastoma BE(2)-C cellsEnviron Health Prev Med172012246251

 PubMedGoogle Scholar

L.RayP.KumarK.C.GuptaThe activity against Ehrlich's ascites tumors of doxorubicin contained in self assembled, cell receptor targeted nanoparticle with simultaneous oral delivery of the green tea polyphenol epigallocatechin-3-gallateBiomaterials34201330643076

 PubMed Web of Science ®Google Scholar

S.H.LeeH.J.NamH.J.KangH.W.KwonY.C.LimEpigallocatechin-3-gallate attenuates head and neck cancer stem cell traits through suppression of Notch pathwayEur J Cancer49201332103218

 PubMed Web of Science ®Google Scholar