EGCG对结肠癌HT-29细胞生长的影响及机制  

Effects of epigallocatechin-3-gallate on human colon cancer cell line HT-29 in vitro

作　　者：张淳[1] 周萍[1] 陈卫昌[2] 

机构地区：[1]无锡市第三人民医院,江苏无锡214000 [2]苏州大学附属第一医院

出　　处：《山东医药》2008年第26期6-8,共3页Shandong Medical Journal

基　　金："江苏省135重点医学人才"基金资助项目(RC2007076)

摘　　要：目的探讨表没食子儿茶素没食子酸酯(EGCG)对人结肠癌细胞株HT-29生长的影响及可能作用机制。方法采用不同浓度的EGCG处理HT-29细胞,四唑盐比色试验(MTT)法观察处理后细胞的生长情况;流式细胞术(FCM)检测细胞凋亡情况;Western Blot洁检测表皮生长因子受体(EGFR)、细胞外信号调节激酶(ERK)磷酸化水平的表达。结果EGCG处理后HT-29细胞生长明显抑制,呈现时间、剂量依赖性;HT-29细胞凋亡率升高;EGFR和ERK的磷酸化水平表达下调。结论EGCG可明显抑制结肠癌HT-29细胞的生长;其可能机制为下调EGFR和ERK的磷酸化水平,从而干预EGFR-ERK信号转导通路。Objective To study the effects of epigallocatechin-3-gallate（EGCG） on human colon cancer cell line HT-29 in vitro and its mechanism. Methods In vitro, human colon cancer cell line HT-29 was treated with EGCG at different level, and then the proliferation of cell was assayed by MTT method. Cell cycles and apoptosis were analyzed by flow cytometry（FCM）. The expression of EGFR were analyzed by Western blot. Results After treated by EGCG, the proliferation of HT-29 cell was inhibited in dose-and-time dependent manner, and the cell apoptosis increased, the phosphorylated forms of EGFR and ERK decreased. Conclusion EGCG can inhibit the growth of HT-29 cell in dose- and-time dependent manner, and the mechanisms maybe downregulated the phosphorylated forms of EGFR and ERK which related to EGFR-ERK signal transduction pathway.

关 键 词：结肠肿瘤 结肠癌 表没食子儿茶素没食子酸酯 表皮生长因子受体 细胞外信号调节激酶 

分 类 号：R735.3[医药卫生—肿瘤]