Livin通过Akt信号途径促进胃癌SGC7901细胞的上皮细胞间质转换  

Livin promotes epithelial-mesenchymal transition of SGC7901 cells through AKT signaling

作　　者：张生军[1] 常琦[1] 刘勇峰[1] 刘敏丽[2] 

机构地区：[1]延安大学附属医院普外科,陕西延安716000 [2]延安大学附属医院病理教研室,陕西延安716000

出　　处：《基础医学与临床》2016年第5期586-589,共4页Basic and Clinical Medicine

基　　金：陕西省教育厅自然科学研究项目(09JK819)

摘　　要：目的探讨胃癌SGC7901细胞中Livin基因的表达对细胞上皮细胞间质转换(EMT)的影响。方法用Livin基因的shRNA慢病毒感染胃癌SGC7901细胞,筛选稳定沉默的细胞株,Transwell检测细胞的侵袭能力,细胞划痕实验检测细胞迁移能力,Western blot检测E-cadherin和vimentin表达,同时检测Akt信号通路的激活状态。结果沉默Livin基因后,胃癌SGC7901细胞侵袭迁移能力明显降低(P<0.05),E-cadherin明显上调,vimentin则明显下调(P<0.05),同时明显抑制Akt信号通路信号的激活(P<0.05)。结论 Livin能够通过激活Akt信号通路从而诱导SGC7901细胞发生EMT,从而促进肿瘤细胞体外侵袭及迁移能力。Objective To investigate whether livin expressed in gastric cancer SGC7901 cells may affect epithelialmesenchymal transition （EMT）. Methods SGC7901 cells were infected with livin shRNA lentivirus, stable transfection cells were selected. The invasion and migration of the stable transfection cells were detected by Transwell and Wound healing assay. The protein of E-cadherin and Vimentin was detected by Western blot. The activation of Akt signaling was detected by Western blot. Results Silencing livin in SGC7901 cells inhibited invasion and migrationin vitro （ P 〈 0. 05 ）. The protein of E-cadherin was significantly increased and vimentin was significantly decreased when livin was silenced by livin shRNA （ P 〈 0.05 ）. Also, the activation of Akt signaling was significantly decreased （ P 〈 0. 05 ）. Conclusions Livin expressed in gastric cancer cell promotes invasion and migration ability in vitro through induction of EMT by activation of AKT signaling.

关 键 词：SHRNA LIVIN EMT 

分 类 号：R735.2[医药卫生—肿瘤]