MiR-21通过PTEN/PI3K/AKT信号通路抑制胰腺癌细胞系生长侵袭能力的体外研究  

Mi R-21 inhibits proliferative and invasive abilities of human pancreatic adenocarcinoma cell line in vitro through PTEN/PI3K/AKT signaling pathway

作　　者：孙吉春[1] 黄飞舟[1] 聂晚频[1] 刘浔阳[1] 冯超[1] 

机构地区：[1]中南大学湘雅三医院普外科,湖南长沙410013

出　　处：《中国现代医学杂志》2015年第12期39-44,共6页China Journal of Modern Medicine

基　　金：湖南省科技厅计划(No:2012FJ4075)

摘　　要：目的探讨Mi R-21对胰腺癌细胞生长和侵袭的影响。方法采用脂质体Lipofectamine 2 000将Mi R-21 inhibitor和Mi R-21 inhibitor阴性对照转染至胰腺癌细胞ASPC-1,q RT-PCR检测转染效果,细胞免疫荧光、Western blot检测转染后目的蛋白的表达,Transwell、划痕实验检测细胞迁移侵袭能力,MTT法检测细胞的增殖活性,流式细胞术检测细胞周期分布的改变。结果成功构建稳定下调Mi R-21的胰腺癌细胞亚系ASPC-1-Mi R-21,荧光定量PCR结果显示Mi R-21表达量明显下调,抑制Mi R-21表达后ASPC细胞的侵袭和增殖能力均受到明显抑制;抑制Mi R-21能明显增强PTEN蛋白和减低p-AKT蛋白表达水平,对AKT蛋白水平无明显影响。结论抑制Mi R-21表达可能通过调控PTEN/AKT通路抑制胰腺癌细胞ASPC-1增殖和侵袭。[Objective]To investigate the effects of the micro RNA 21（mi R-21） on the growth and invasion of pancreatic adenocarcinoma cells.[Methods]Mi R-21 inhibitor and mi R-21 inhibitor negative control were transfected into human pancreatic adenocarcinoma cell line ASPC-1 by Lipofectamine 2000. The transfection efficiency was detected by real-time PCR. The target protein was detected by Western blot. Finally, scratch test, transwell cell invasion, MTT and flow cytometry were used to detect the migratory, invasive, and proliferative activities of the tumor cells. [Results]A cell subclone stably expressing a low level of mi R-21 was obtained and verified by real-time quantitative PCR. Suppressed Mi R-21 significantly inhibited the invasion and proliferation of ASPC-1 cells. Inhibition of mi R-21 did not affect the expression of total AKT, whereas the phosphorylated AKT level was markedly down-regulated and the PTEN protein expression was up-regulated. [Conclusions]Suppression of mi R-21 could inhibit the migration and proliferation of human pancreatic adenocarcinoma cell line ASPC-1 via the PTEN/PI3K/AKT pathway.

关 键 词：MIR-21 PTEN/PI3K/AKT 胰腺癌 侵袭 增殖 

分 类 号：R735.9[医药卫生—肿瘤]