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

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cyclinD1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。

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

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.MethodsCell 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.ResultsAkt 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.ConclusionThe 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.