Inhibitory effect of rapamycin on PI3K/AKT/mTOR signaling pathway in gastric adenocarcinoma MGC-803 cells

Objective To investigate the effect of rapamycin on growth of gastric carcinoma cell line MGC-803 and to explore its possible mechanism.Methods Human gastric cancer cell line MGC-803 cells were cultured in vitro and treated with rapamycin of different concentrations.The proliferation of MGC-803 cells was detected with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay;the expressions of mRNA of relevant genes were determined with quantitative real-time PCR (QPCR) and the expressions of related proteins were detected with Western blot;the changes in cell cycle and apoptosis were measured with flow cytometry.Results Compared to that of the control group,the proliferation of MGC-803 cells treated with rapamycin was downregulated in a dose-dependent manner (P<0.05).Rapamycin significantly downregulated the expressions of mRNA of phosphatidylinositol 3-kinase (PI3K),protein kinase B (AKT),mammalian target of rapamycin (mTOR),4EBP,and P70S6K (P<0.05 for all).Rapamycin downregulated expressions of p-mTOR and p-P70S6K.The cell cycle of MGC-803 cells treated with rapamycin was arrested mainly in the G0/G1 stage,and apoptosis of the MGC-803 cells was observed (P<0.05).Conclusion Rapamycin can inhibit the grouth of MGC-803 cells by regulating the PI3K/AKT/mTOR signaling pathway.