Effect Of Rapamycin On Human Gastric Carcinoma SGC7901 Cells Proliferation And Approach Of The Mechanisms

Objective To investigate the effects of Rapamycin on cell proliferation in human gastric carcinoma SGC7901 cells and the potential mechanisms involved in the inhibitory effects of the mTOR signaling pathway. Provide the new ideas and original strategy about the drug treatment for human gastric carcinoma.Methods SGC7901 cells were cultured in vitro.The expression of mTOR and HIF-1αproteins was determined by immunocytochemical method in SGC7901 cells cultured under hypoxic conditions.Different concentrations of Rapamycin were incubated with SGC7901 cells for 12 hours,24 hours,48 hours and 72 hours. Cell proliferation was measured by CCK-8 assay in Rapamycin—treated SGC7901 cells.The expression levels of mTOR and HIF—lαmRNA was detected by semi-quantitative RT-PCR.The change of mTOR and HIF—lαproteins was determined by Western Blot.The experimental data were processed by SPSS13.0 .Results Immunocytochemistry showed that under hypoxic conditions ,mTOR was positively expressed in the cytoplasm and that HIF—lαin the nucleus and cytoplasm of SGC7901 cells. Rapamycin could significantly inhibit the proliferation of SGC7901 cells in a concentration-dependent and time- dependent manner.The expression levels of mTOR,HIF—lαmRNA and mToR,HIF—lαproteins were significantly lower in Rapamycin—treated SGC7901 cells than those in untreated cells.Conclusions mTOR/HIF—lαsignaling pathway is abnormally activated in SGC7901 cells under hypoxic conditions.Rapamycin could significantly inhibit the proliferation of SGC7901 cells in vitro possibly by downregulating mTOR/HIF—lαsignaling pathway under hypoxic microenvironment of tumor.