Six1通过PI3K通路抑制肺癌细胞A549的增殖和迁移  

Six1 inhibits the proliferation and migration of A549 cells through PI3K pathway

作　　者：陈炆颖[1] 蔡少鑫[1] 洪如钧[1] 林明[1] 陈愉生[1] 

机构地区：[1]福建省立医院急诊内科,福州350001

出　　处：《福建医药杂志》2014年第5期56-59,共4页Fujian Medical Journal

摘　　要：目的研究Six1基因对人肺癌细胞A549增殖和迁移能力的影响及其作用机制。方法将Six1的特异小干扰RNA序列转染入A549细胞中,应用Western印迹法检测Six1在A549细胞中的蛋白水平的表达情况,应用MTT法和细胞计数观察低表达Six1对A549细胞增殖的作用,应用划痕实验和transwell侵袭小室实验检测A549细胞迁移能力的变化情况,应用Western印迹法检测PI3K信号通路蛋白的表达变化。结果在A549细胞中,特异的小干扰RNA使Six1在蛋白水平表达降低,低表达Six1的A549细胞系增殖和迁移能力下降,p-AKT的蛋白表达降低。结论在A549细胞系中Six1通过PI3K通路抑制A549细胞的侵袭和转移能力。Objective To investigate the influence of Six1 on cell proliferation and migration in A549 cell line and its mechanism.Methods Six1 specific Si-RNA was transfected into human lung carcinoma cell line A549.We detected the efficiency of transfection by Western blot.The effects of si-Six1 on A549cell growth was by means of MTT and cell count assay;The effects of Six1 on A549cell migration was by means of cell scratch test and transwell assay;The protein expression of PI3 KSignal pathway was detected by western blot.Results In A549 cell line,the expression of Six1 was knocked-down by specific siRNA,and down-regulation of Six1 decreased the expression of p-AKT,which led to decrease of the ability of proliferation and migration of A549.Conclusion Six1 inhibits the proliferation and migration of A549 cells through PI3 Kpathway.

关 键 词：肺癌 Six1 PI3K通路 增殖和侵袭 

分 类 号：R734.2[医药卫生—肿瘤]