高迁移率族蛋白B1在诱导肝癌细胞HepG2发生上皮间质转换中的作用

The role of high mobility group box 1 in epithelial mesenchymal transition in hepatocellular carcinoma cell line HepG2

目的探讨高迁移率族蛋白B1(high mobility group box 1,HMGB1)在血管紧张素Ⅱ(AngiotensinⅡ,AngⅡ)诱导肝癌细胞上皮间质转化(epithelial mesenchymal transition,EMT)过程中的关键作用。方法使用AngⅡ刺激肝癌细胞系HepG2,分别通过转染HMGB1过表达质粒和siRNA上调和下调HMGB1表达,检测HepG2中相关EMT基因和蛋白的表达变化。结果将成功构建的HMGB1稳定过表达和HMGB1表达抑制的HepG2做细胞划痕、Transwell和Western blot验证EMT过程相关蛋白的变化,结果显示与阴性对照相比,HMGB1高表达的肝癌细胞经AngⅡ处理后,侵袭和迁移能力增强,E-钙黏蛋白(E-cadherin)蛋白表达下调,波形蛋白(Vimentin)表达上调;与阴性对照相比,HMGB1干扰的肝癌细胞经AngⅡ处理前后,侵袭和迁移能力差异无统计学意义,E-cadherin和Vimentin表达差异无统计学意义。结论HMGB1可以促进AngⅡ诱导肝癌细胞HepG2发生EMT。

Objective To investigate the role of high mobility group box 1(HMGB1)in angiotensinⅡ(AngⅡ)-induced epithelial mesenchymal transition(EMT).Methods HepG2 cells were stimulated by AngⅡ,and transfected by HMGB1 over expressed plasmid or HMGB1 siRNA separately.EMT related proteins were examined to assess the effect of HMGB1.Results We successfully constructed the over expression plasmid of HMGB1 and siRNA of HMGB1,and transfected to HepG2 cells.The invasion and migration abilities of HMGB1 over expressed cells under the treatment of AngⅡwere significantly increased compared with negative controls(NC);and E-cadherin was down-regulated while vimentin was up-regulated Compared with NC,the invasion and migration abilities of HMGB1 siRNA cells under the treatment of AngⅡhad not changed,and the expression of E-cadherin and Vimentin was constant.