首页> 中文期刊> 《癌症进展》 >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

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

         

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、mTOR蛋白及mRNA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、mTOR蛋白及mRNA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mTOR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.

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