抑制PI3K/Akt信号通路对胃癌细胞转移和侵袭影响的研究  

Effects of PI3K/Akt inhibition on the metastasis and invasion of human gastric carcinoma cell SGC-7901 and its mechanism

作　　者：王艳丽[1] 高青[2] 

机构地区：[1]重庆市第三人民医院消化内科,重庆400014 [2]重庆医科大学附属第一医院消化外科,重庆400016

出　　处：《重庆医科大学学报》2011年第1期27-30,共4页Journal of Chongqing Medical University

摘　　要：目的:探讨PI3K/Akt信号通路对胃癌细胞转移和侵袭的影响。方法:选用PI3K/Akt信号通路抑制剂LY294002体外作用于胃癌细胞株SGC-7901,Western blot检查总Akt和p-Aktser473蛋白表达,细胞粘附实验观察细胞与基质的粘附力,Transwell法检查细胞侵袭能力,RT-PCR及免疫细胞化学法检查E-cadherin mRNA及蛋白表达。结果:经LY294002处理的SGC-7901,总Akt表达无改变,p-Aktser473蛋白表达下降;细胞与基质的粘附力及侵袭能力减弱;E-cadherin mRNA及蛋白表达水平升高。结论:抑制PI3K/Akt信号通路可减弱胃癌细胞的转移、侵袭能力,其可能机制与上调E-cadherin表达相关。Objective：To investigate the influence of PI3K/Akt on metastasis and invasion of human gastric carcinoma.Methods：Human gastric carcinoma cell line SGC-7901 was cultured with PI3K/Akt signaling pathway inhibitor LY294002 in vitro.The expression of total Akt and p-Aktser473 were detected in protein level by Western blot,the cell-ground substance adhesion was tested by cell adherence assay and the invasion ability was measured with Transwell plate,the expression of E-cadherin in mRNA level and protein level were detected by RT-PCR and S-P immunohistochemistry.Results：The expression of total Akt was constant,but the protein level of p-Aktser473 was down regulated after treatment with LY294002,the adhesion rate and the invasion ability were decreased,the expression of E-cadherin in mRNA and protein were positively regulated.Conclusion：The metastasis and invasion capacity of human gastric carcinoma cell could be decreased by inhibiting PI3K/Akt,perhaps the mechanism is associated with increasing of E-cadherin expression.

关 键 词：胃癌 转移 侵袭 钙黏蛋白E 

分 类 号：R735.2[医药卫生—肿瘤]