PI3K/mTOR双重抑制剂Bez235抑制SGC-7901胃癌细胞增殖的作用  

Bez235,Inhibitor of Phosphoinositol-3-kinase/mTOR,Inhibits SGC-7901 Cell Proliferation

作　　者：彭方[1] 张艳强[1] 许广群[1] 郭爱军[2] 王凤泽[3] 

机构地区：[1]泰山医学院基础医学院,山东泰安271016 [2]泰安市中心医院放射科 [3]泰山医学院生物科学学院

出　　处：《肿瘤防治研究》2012年第11期1294-1296,共3页Cancer Research on Prevention and Treatment

基　　金：国家自然科学基金资助项目(30800422);泰山医学院博士启动基金资助项目(1378)

摘　　要：目的探讨PI3K/mTOR双重抑制剂Bez235对SGC-7901胃癌细胞增殖和凋亡的影响。方法采用MTT法检测Bez235对SGC-7901细胞增殖的影响;流式细胞术分析细胞周期变化;AnnexinⅤ-FITC试剂盒检测细胞凋亡;免疫印迹法检测蛋白表达水平。结果 MTT结果显示Bez235抑制了SGC-7901细胞的增殖,Bez235作用后使细胞阻滞于G1期,但对SGC-7901细胞凋亡的诱导作用不明显;免疫印迹结果表明,Bez235抑制了SGC-7901细胞中β-catenin的表达,同时抑制了其下游因子cy-clinD1的蛋白水平。结论 PI3K/mTOR抑制剂Bez235对SGC-7901胃癌细胞的增殖具有明显的抑制作用,其机制可能与其调节β-catenin通路相关。Objective To detect the effect of Bez235,inhibitor of phosphoinositol-3-kinase/Akt and mammalian target of rapamycin（mTOR）,on the cell proliferation and apoptosis in human gastric cancer cell line SGC-7901 cells.Methods Cell growth inhibition was detected by MTT assay,cell cycle was analyzed by flow cytometry,AnnexinⅤ-FITC apoptosis detection kit was used to detect apoptosis of cells,protein expression was examined by Western blot analysis.Results Akt phosphorylation was dose-dependently inhibited by Bez235 in SGC-7901 cells.MTT and cell cycle analysis results indicated that Bez235 inhibited the growth of SGC-7901 cells in a dose-dependent manner,Bez235 arrested cell cycle progression at the G1 phase.The level of β-catenin and cyclinD1,a downstream protein of β-catenin,was down-regulated after Bez235 treatment.Conclusion The dual PI3K/mTOR inhibitor Bez235 shows substantial anti-tumor activity in SGC-7901 cells,and β-catenin pathway maybe potentially contributed to the anticancer activity of Bez235.

关 键 词：Bez235 PI3K Akt 细胞增殖 Β-CATENIN 

分 类 号：R735.2[医药卫生—肿瘤]