The Experimental Studies Of Effect And Its Mechanism Of MTOR Inhibitors On Human Gastric Cancer Cell Lines

Objective: Researching the effects and analyze the molecular mechanism of mTORinhibitors on gastric cancer cell lines.Method: Firstly, we use rapamycin and PP242on gastric cancer cell lines, observingthe effects of growth characteristics on the gastric cancer cell lines, and understand itsmechanism by observing the relevant pathl proteins. Secondly, we use MEK inhibitorU0126joining rapamycin and PP242to deal with gastric cancer cell lines, to observe theeffects of growth characteristics of combination inhibitors on gastric cancer cell lines, andunderstand the mechanism by observing the relevant path proteins.Result: After rapamycin and PP242separately used on gastric cancer cell lines, wefound that two are three cell lines were sensitive to both rapamycin and PP242, while theremaining five cell lines were not sensitive to both. Then we observed the mTOR pathwayproteins after mTOR inhibitors used on gastric cancer cell lines, rapamycin had feedback p-AKT473quantity increased, whereas the PP242group could obviously decrease theexpression of p-AKT473, but it could cause the activation of MAPK pathway. So we useMEK inhibitor U0126joining rapamycin and PP242to deal with gastric cancer cell lines atthe same time, and the results showed that the inhibition rates of gastric cancer cell linewas significantly enhanced, by observing the mTOR pathway proteins,we could see thatU0126joining mTOR inhibitors could obviously decrease the expression of p-ERK.Conclusion: Negative feedback p-AKT473increasing and MAPK pathway activationmay be the important mechanism of gastric cancer cell line resist to mTOR inhibitors, andthe combination mTOR inhibitors with MEK inhibitors could more significantly inhibit thegrowth of gastric cancer lines.