干扰ELK-3抑制人肝癌细胞的上皮-间质转换  

ELK-3 interference inhibits the epithelialmesenchymal transition of human hepatocellular carcinoma cells

作　　者：李天柱[1] 史铁伟[1] 周静[1] 金光虎[1] 张俊毅[1] 郝丹丹[1] 白春英[1] LI Tian-zhu SHI Tie-wei ZHOU Jing JIN Guang-hu ZHANG Jun-yi HAO Dan-dan BAI Chun-ying(Molecular Medicine Research Center, Chifeng Medical College, Chifeng University, Chifeng 024000, Chin)

机构地区：[1]赤峰学院医学院分子医学研究中心,内蒙古赤峰024000

出　　处：《基础医学与临床》2017年第2期211-216,共6页Basic and Clinical Medicine

基　　金：内蒙古自然科学基金(2015MS0801)

摘　　要：目的研究转录因子ELK-3与人肝癌细胞系Hep G2和Hu H7上皮-间质转换(EMT)的关系及其作用机制。方法将Hep G2和Hu H7细胞分为小干扰RNA转染组和Ras-ELK-3信号通路抑制剂(XRP44X)处理组。用Western blot检测ELK-3、ELK-3靶基因EGR-1以及EMT相关分子钙黏附素E(E-cadherin)、波形蛋白(vimentin)的表达和MAPK信号通路蛋白p38的表达。结果 ELK-3干扰或Ras-ELK-3信号通路抑制剂(XRP44X)处理肝癌细胞后其ELK-3和ELK-3的靶基因EGR-1的蛋白表达均显著降低(P<0.01),E-cadherin表达水平升高(P<0.01),vimentin的表达及p38磷酸化水平均降低(P<0.01)。结论通过干扰ELK-3下调p38抑制EMT。Objective To investigate the relationship of ELK-3 and epithelial-mesenchymal transition（ EMT） for exploring its possible mechanism. Methods The human hepatocellular carcinoma cells（ HCC） were divided into small interference RNA transfection group and Ras-ELK-3 pathway inhibitor group. The protein level of ELK-3 target gene EGR-1 E-cadherin,vimentin and p38 in HCC were determined by Western blot analysis. Results The protein level of ELK-3 and its target gene EGR-1 in treated human hepatocellular carcinoma cells significantly decreased as compared with the negative control group（ P〈0. 01）. The protein level of E-cadherin was significantly increased（ P〈0. 01）,while vimentin and p38 were decreased in HCC cells with ELK-3 interference（ P〈0. 01）. Conclusions ELK-3 interference can inhibit the epithelial- mesenchymal transition of HCC cells by down-regulating p38.

关 键 词：ELK-3 肝癌细胞 上皮间质转换 P38 

分 类 号：R735.7[医药卫生—肿瘤]