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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

机译:绿茶EGCG诱导Akt,ERK1 / 2和p38MAPK信号通路在大肠癌细胞凋亡中的意义

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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 -p38 alpha, -p38 gamma and -p38 delta, as well as phospho-Alct 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 anticancer effects of EGCG and indicate potential use of this compound as chemotherapeutic agent for colon cancer treatment (C) 2015 Elsevier Ltd. All rights reserved.
机译:我们调查了由绿茶成分Epigallocatechin-3-gallate(EGCG)诱导的细胞凋亡及其在结肠癌细胞系中的潜在活性通路。对绿茶多酚靶向的机制和分子的全面理解可能有助于开发新的癌症治疗方法。 EGCG是绿茶中的主要多酚,在HT-29细胞死亡中具有细胞毒性作用并诱导细胞死亡。在这项研究中,我们评估了EGCG对有丝分裂原激活的蛋白激酶(MAPK)和Akt途径的影响。 EGCG处理增加了磷酸-ERK1 / 2,-JNK1 / 2和-p38α,-p38γ和-p38δ以及磷酸-Alct的水平。使用激酶抑制剂的组合,我们发现通过抑制Akt,ERK1 / 2或其他p38MAPK活性,可以部分阻止EGCG诱导的细胞死亡。我们的数据表明,这些激酶途径与EGCG的抗癌作用有关,并表明该化合物作为结肠癌治疗的化学治疗剂的潜在用途(C)2015 Elsevier Ltd.保留所有权利。

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