Research Of Function And Mechanism Of MiR-506by Targeting Gli3in Human Cervical Cancer

[Objective] By the investigation of the expression level and biological function ofmiR-506in cervical cancer tissues and cells, we would explore the mechanism ofmiR-506targeting Gli3of Hedgehog signaling pathway.[Methods](1) We evaluated miR-506and Ki67expression in50matched pairs ofcervical cancer and corresponding non-tumorous cervical tissues using real-time PCR,compared the difference and analyzed the trend; we analyzed the correlation of theexpression level between miR-506and Ki67by Spearman correlation; we gain-orloss-miR-506to explore its biological function of in cervical cancer by the detectionof the proliferation, cell cycle, apoptosis, caspase3/7activity, paclitaxel and cisplatinsensitivity.(2) We would explore whethermiR-506could regulate Gli3bydualluciferase reporter gene system; we gain-or loss-Gli3to investigate whether thebiological function of miR-506was recapitulated or antagonized by the detection ofthe proliferation, cell cycle, apoptosis, caspase3/7activity, paclitaxel and cisplatinsensitivity.[Results](1) miR-506expression was clearly down-regulated in cervical cancertissues compared with non-tumorous cervical tissues; miR-506expression wasinversely correlated with Ki-67in these clinical samples; miR-506mimics couldinhibit cancer cell proliferation, reduce caspase3/7activity, increasechemosensitivity, block G1/S transition and promote apoptosis, knockdown ofmiR-506obtained the opposite results.(2) Gli3was one of target genes of miR-506by dual luciferase reporter gene system; gain-or loss-Gli3could recapitulate orantagonize these biological functions induced by miR-506.[Conclusions] Theexpression of miR-506was downregulated in cervical cancer. miR-506exerts itsanti-proliferative function by directly targeting Gli3. This newly identifiedmiR-506/Gli3axis provides further insight into the pathogenesis of cervical cancerand indicates a potential novel therapeutic agent for the treatment of cervical cancer.