The Effect Of MiR-100 On Autophagy And Apoptosis And Proliferation Of Endometrial Adenocarcinoma Cells

Objective: The aim of this study was to investigate the effect of miR-100 on the autophagy,proliferation and apoptosis of KLE cells in poorly differentiated and well-differentiated endometrial adenocarcinoma cells.And to explore the relationship between miR-100 and the development of endometrial adenocarcinoma and the regulation of mTOR signaling pathway on cell proliferation and apoptosis,and to investigate the effect of miR-100 on endometrial adenocarcinoma Early diagnosis and treatment to provide a new theoretical basis.Methods: The expression of miR-100 in the mimics group was higher than that in the NC-mimics group and the mock group,and the miR-100 inhibitor group was lower than that in the NC-inhibitor group and the mock group.The miR-100 mimics group Compared with NC-mimics group and mock group,the expression of Beclin1 and LC3 was higher in miR-100 inhibitor group than in NC-inhibitor group and mock group.The miR-100 inhibitor group was lower than NC The cell viability of miR-100 inhibitor group was significantly lower than that of NC-inhibitor group and mock group.The survival rate of KLE cells was significantly higher than that of the control group(P <0.05),and the survival rate of KLE cells was significantlyhigher than that of the control group The expression of LC3 and Beclin1 protein in miR-100 inhibitor group was significantly lower than that in NC-inhibitor and mock group.After transfection with miR-100 inhibitor,mTOR inhibitor rapamycin could restore miR-100 inhibitor on cell proliferation,but also to restore miR-100 inhibitor-induced apoptosis.Results:The expression of miR-100 in miR-100 mimics group was significantly higher than that in NC-mimics group and mock group,and miR-100 inhibitor group was significantly higher than that in NC-inhibitor group and mock group.The expression of Beclin1 and LC3 in miR-100 mimics group was higher than that in NC-mimics group and mock group.Compared with NC-inhibitor group and mock group,the levels of autophagy genes Beclin1 and LC3 were lower in miR-100 mimics group.The expression of miR-100 inhibitor group was higher than that of NC-inhibitor group and mock group,and the apoptosis of KLE cells was increased in miR-100 mimics group compared with NC-mimics group and mock group.After 48 hours of transfection of KLE cells,The survival rate of miR-100 inhibitor group was higher than that of NC-inhibitor group and mock group,and the survival rate of miR-100 mimics group was lower than that of NC-mimics group and mock group.After transfection of KLE cells,WB The expression of LC3 and Beclin1 protein in miR-100 mim group was significantly lower than that in NC-mimics group and mock group(P <0.05),and the expression of LC3 and Beclin1 protein in miR-100 mimics group was higher than that in NC-mimics group and mock group;After transfection of miR-100 inhibitor,add mTOR inhibitor rapamycin Can reduce the effect of miR-100 inhibitor on cell proliferation in KLE cells and also promote the inhibition of apoptosis induced by miR-100 inhibitor.Conclusion: Downregulation of miR-100 resulted in decreased KLE autophagy and inhibition of apoptosis but promote cells proliferation in endometrial adenocarcinoma cells,but promoted the proliferation of miR-100 when miR-100 target receptor mTOR was inhibited by rapamycin Cell proliferation and ultimately inhibit cell proliferation and restore miR-100down-regulation induced apoptosis and promote apoptosis,so consider the miR-100 by targeting mTOR regulation of endometrial adenocarcinoma cell autophagy,withered Death and proliferation process,when the miR-100 down,inhibition of autophagy,inhibition of apoptosis,promote cell proliferation,leading to the occurrence of endometrial adenocarcinoma.