Table 1 The effects of EGCG in different cancers
From: Epigallocatechin-3-gallate and cancer: focus on the role of microRNAs
Cancer | Dose (s) | Mechanism | Model (In vitro/ In vivo) | Cell line | Refs. |
|---|---|---|---|---|---|
Glioma | 82 and 134 μg/mL | Decrease the guidance of axon process and different metabolic-related pathways | In vitro | 1321N1 | [40] |
Ovarian cancer | 5–80 μg/mL | -Increasing the activity of Bax and caspase-3 -Decreasing the activity of Bcl-2 | In vitro | NIH-OVCAR-3, SKOV3, and CAOV-3 | [41] |
Gastric cancer | 25, 50, 100, 200, 400, 800 μg/ml | Decrease HBV infection | In vitro | HepG2.2.15 | [42] |
Gastric cancer | 12.5, 25, 50, 100, 200 μM | Increase autophagy | In vitro | HepG2, HepG2.2.15 | [43] |
Gastric cancer | 0–100 μg/ml | Decrease proliferation and increase apoptosis | In vitro | HepG2 | [44] |
Gastric cancer | 0–150 μM | Increase autophagy | In vitro | HepG2 | [45] |
Breast cancer | 5 -20 μg/mL | Increase the control of caspase-9, caspase-3, PARP | In vitro | MCF-7 | [9] |
Breast Cancer | 5 μM | The suppression of N-cadherin | In vitro | HCC1806, MDA-MB-231, MDA-MB-157, MCF-7, | [46] |
Endometrial cancer | 20- 60 μM | Reduce the activity of Akt/ PI3K/mTOR/HIF-1α pathway to inhibit control of HIF-1α/VEGFA | In vitro | AN3CA, PHES, THP-1, RL95-2, | [47] |
Breast cancer | 10–320 μM | Increased control of caspase-9, caspase-8, caspase-3 | In vitro | 4 T1 | [48] |
Breast cancer | 20–120 μmol/L | Decreasing the activity of the p53 /Bcl-2 pathway | In vitro | MCF-7 | [49] |
Breast cancer | 0–80 μM | Reduce control of the PI3K /Akt pathway | In vitro | T47D | [50] |
Breast cancer | 40Â nmol | Focus on pathways that either promote vascular growth or programmed cell death | In vitro | Hs578T | [51] |
Breast cancer | 25- 100 mg/L | Reduce the control of VEGF and HIF-1α | In vitro | MCF-7 | [52] |
Breast cancer | 10- 50 ug/mL | Decrease control of HIF-1α, NF-κB | In vitro | MCF-7, E0771 and MDA-MB- 231 | [31] |
Ovarian cancer | 20–100 μg/ mL | Reduce control of AQP5, NF-κB, IκB-α and p65 | In vitro | SKOV3 | [27] |
Endometrial cancer | 100 μM | The blocking of MAPK and Akt pathways | In vitro | Ishikawa cells | [53] |
Breast cancer | 5–20 μM | Reducing the activity of the ERK/NF-κB/PI3K pathway | In vitro | MCF-7 | [54] |
Breast cancer | 25–100 μM | The Wnt pathway and its target gene c-MYC can be suppressed | In vitro | MDA-MB-231 | [30] |
Ovarian cancer | 20–40 μmol/L | Lessen the control of ETAR-influenced processes | In vitro | HEY and OVCA 433 | [55] |
Ovarian cancer | 25- 100 μM | The expression of p21 can be increased, while the expression of PCNA and Bcl-xL can be reduced, and Bax can be elevated | In vitro | SKOV-3, OVCAR-3, PA-1 | [56] |
Ovarian cancer | 50 mg/kg | Prevents the development of cancer by controlling the activity of PTEN/mTOR/Akt pathway | In vivo | – | [41] |
Glioma | 87Â mg/kg | Induce apoptosis | In vivo, In vitro | C6 | [57] |
Breast cancer | 300 μg | DNMT2 methylation activity is inhibited | In vivo | – | [58] |
Breast cancer | 50–100 mg/ kg | Suppresses cancer VEGF expression | In vivo | – | [31] |
Endometrial cancer | 50 mg/kg | Preventing cancer angiogenesis and growth | In vivo | – | [59] |
Endometrial cancer | 65 mg/kg | The suppression of VEGF has been demonstrated | In vivo | – | [60] |
Ovarian cancer | 12.4 g/L | Reducing the amount of ETAR and ET-1 in cancer cells has been shown to impede their growth | In vivo | – | [55] |