胃癌细胞SGC7901凋亡的PI3K/Akt通路介导作用及雷帕霉素的作用机制分析  

Role of rapamycin in the PI3K/AKT mediated apoptosis of SGC7901 cell line

作　　者：宋仕茂[1] 陈宇[1] 张治国[1] 骆志国[1] 

机构地区：[1]湖北医药学院附属太和医院肿瘤科,湖北十堰442000

出　　处：《癌症进展》2016年第6期601-604,共4页Oncology Progress

摘　　要：目的分析雷帕霉素对胃癌细胞中PI3K/Akt蛋白表达的影响作用,以为临床治疗提供参考。方法将生长状态良好的胃癌细胞SGC7901随机分为4组:对照组,雷帕霉素低剂量组、中剂量、高剂量组(n=8)。采用DAPI染色法分析各组细胞的凋亡情况;采用免疫印迹法和Real-time PCR检测PI3K/AKT信号通路中相关蛋白PI3K、AKT、m TOR蛋白及m RNA的表达。结果雷帕霉素低、中、高剂量组均可抑制细胞的增殖,差异具有统计学意义(P﹤0.05);雷帕霉素下调了胃癌细胞中PI3K、AKT、m TOR蛋白及m RNA的表达,且与对照组比较,差异均有统计学意义(P﹤0.05)。结论雷帕霉素主要通过抑制PI3K、AKT及m TOR的过表达发挥肿瘤抑制作用。Objective To explore the role of rapamycin in the apoptosis of SGC7901 cell line which is mediated by PI3K/AKT signaling pathway. Method SGC7901 cell line were randomized into 4 groups as control group, and treat-ment groups of rapamycin with low, medium and high dose （n=8）. The apoptosis of cell line in each group was detected by DAPI staining;western blotting and real-time PCR tests were utilized in determining the expression of related proteins as PI3K, AKT, mTOR and mRNA in PI3K/AKT signaling pathway. Result Rapamycin could induce apoptosis of SGC7901 cell line in a dose dependent and time dependent manner, with statistically significant differences observed （P〈0.05）;the expression of PI3K, AKT and mTOR in SGC7901 cell line was significantly downregulated by rapamycin as demonstrated in western blotting （P〈0.05）. Conclusion Rapamycin inhibits SGC7901 mainly through restraining the over expression of PI3K, AKT and mTOR.

关 键 词：细胞凋亡 PI3K/AKT信号通路 雷帕霉素 免疫印迹法 

分 类 号：R735.2[医药卫生—肿瘤]