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Implication of Akt, ERK1/2 and alternative p38MAPK signalling pathways in human colon cancer cell apoptosis induced by green tea EGCG

We investigated apoptosis induced by the green tea component the epigallocatechin-3-gallate (EGCG) and the pathways underlying its activity in a colon cancer cell line. A complete understanding of the mechanism(s) and molecules targeted by green tea polyphenols could be useful in developing novel th...

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Published in:Food and chemical toxicology 2015-10, Vol.84, p.125-132
Main Authors: Cerezo-Guisado, María Isabel, Zur, Rafal, Lorenzo, María Jesús, Risco, Ana, Martín-Serrano, Miguel A., Alvarez-Barrientos, Alberto, Cuenda, Ana, Centeno, Francisco
Format: Article
Language:English
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Summary:We investigated apoptosis induced by the green tea component the epigallocatechin-3-gallate (EGCG) and the pathways underlying its activity in a colon cancer cell line. A complete understanding of the mechanism(s) and molecules targeted by green tea polyphenols could be useful in developing novel therapeutic approaches for cancer treatment. EGCG, which is the major polyphenol in green tea, has cytotoxic effects and induced cell death in HT-29 cell death. In this study, we evaluated the effect EGCG on mitogen-activated protein kinase (MAPK) and Akt pathways. EGCG treatment increased phospho-ERK1/2, -JNK1/2 and -p38α, -p38γ and -p38δ, as well as phospho-Akt levels. Using a combination of kinase inhibitors, we found that EGCG-induced cell death is partially blocked by inhibiting Akt, ERK1/2 or alternative p38MAPK activity. Our data suggest that these kinase pathways are involved in the anti-cancer effects of EGCG and indicate potential use of this compound as chemotherapeutic agent for colon cancer treatment. •Evidence supports a preventive role for epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, in cancer.•EGCG-induced cell death on the HT-29 human colon adenocarcinoma cell line.•Akt, ERK1/2 and p38δ pathways are implicated in EGCG-induced cell death.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2015.08.017