Salidroside Inhibits High Glucose-Activated Ishikawa Cell Line

ObjectiveDiabetes is an independent risk factor for endometrial cancer.The purpose of this study is to investigate the effect of high glucose(HG)on the migration,invasion and survival of Ishikawa endometrial carcinoma cell line,and to explore effects and potential mechanisms of salidroside of HG-incubated carcinoma cells.MethodsBioinformatics was used to analyze the expression of AMPK/m TOR pathway in endometrial carcinoma and its relationship with survival rate and pathological stage.Ishikawa endometrial cancer cell line was cultured in vitro to observe the effect of high glucose on the migration,invasion and apoptosis,and the expression of AMPK,phosphorylated AMPK(p AMPK)and m TOR;Furthermore,we investigated the effect of salidroside on HG-induced migration,invasion and apoptosis,and explored the role of AMPK/m TOR pathway by using AMPK inhibitor Compound C.ResultsCompared with adjacent tissues,the expression of AMPK in endometrial carcinoma was decreased,showing a trend of lower expression and higher pathological stage,which was positively correlated with survival rate.Together with higher expression of m TOR and higher pathological stage,indicating negative correlation with survival rate.In vitro,HG promote the migration,invasion and survival of Ishikawa cell line,and reduce the expression of AMPK and phosphorylation(p AMPK),promoting the expression of m TOR.Importantly,salidroside antagonizes the effect of HG on Ishikawa cells,and the antagonistic effects were attenuated by AMPK inhibitor Compound C.ConclusionsHG promote the survival and invasion ability of Ishikawa cell via AMPK/m TOR pathway,through which,salidroside antagonize the effect of HG on Ishikawa cells.