EGCG经PI_3K-AKT信号通路诱导人胃癌BGC-823细胞G1期阻滞  

Induction of Cell Cycle G1 Phase Arrest by Epigallocatechin-3-gallate via Activating PI_3K-AKT Signaling Pathway in Human Gastric Cancer BGC823 Cells

作　　者：陈晓艳[1] 王强[1] 文小玲[2] 箫赪[1] 罗招阳[1] 

机构地区：[1]南华大学肿瘤研究所,湖南衡阳421001 [2]南华大学医学院临床技能中心

出　　处：《南华大学学报（医学版）》2008年第3期310-312,349,共4页Journal of Nanhua University(Medical Edition)

摘　　要：目的探讨表没食子儿茶素没食子酸酯(Epigallocatechin-3-gallate,EGCG)通过PI3K-AKT通路对人胃癌BGC-823细胞周期调控的分子机制。方法采用噻唑蓝比色法(MTT)检测BGC-823细胞的存活率;碘化丙啶(PI)染色流式细胞术(flow cytometry,FCM)检测EGCG处理前后BGC823细胞周期的变化;Western blot检测PI3K-AKT信号传导通路相关蛋白的表达。结果EGCG能够抑制BGC823细胞的生长,且这种抑制作用与诱导BGC823细胞G1期阻滞有关。EGCG可以下调PI3K-AKT信号通路蛋白Akt的磷酸化表达,对通路下游周期相关蛋白cyclinD1的表达也有抑制作用。结论EGCG能够通过活化PI3K-AKT信号通路发挥诱导人胃癌BGC823细胞G1期阻滞的作用。Objective To elucidate the mechanism of proliferation induced by Epigallocatechin - 3 - gallate （EGCG） on human gastric cancer BGC823 cells via PI3K- Akt pathway. Methods The survival rate of BGC823 cells was detected by MTr assay. The change of cell cycle in BGC823 induced by EGCG was detected by FCM using PI staining. Western blot was used to analyze the expression of PI3 K-AKT signal transduction pathway related proteins such as pAkt, CyclinD1 in BGC823 cells after EGCG treatment. Results EGCG inhibited proliferation of BGC823 cells via induced cell cycle G1 phrase arrest. EGCG could decrease the phosphorylation of Akt and inhibit the expression of cyclinD1 which was the downstream protine of PI3K-AKT signal transduction path-way. Conclusion EGCG inducted cell cycle G1 phase arrest by Epigallocatechin-3-gallate via activating PI3 K-AKT signaling in human, gastric cancer BGC823 Cells.

关 键 词：EGCG 胃肿瘤 AKT通路 细胞周期 

分 类 号：R735.2[医药卫生—肿瘤]