MiR⁃216a调节JAK2/STAT3通路抑制卵巢癌细胞的转移和上皮⁃间质转化

MiR⁃216a inhibits metastasis and epithelial⁃mesenchymal transition of ovarian cancer cells by regulating the JAK2/STAT3 pathway

目的本研究旨在探究微小RNA⁃216a(miR⁃216a)是否通过调节Janus激酶2(JAK2)/信号转导和转录激活因子3(STAT3)途径调控卵巢癌(ovarian cancer,OC)细胞的转移和上皮⁃间质转化(EMT)。方法qRT⁃PCR检测卵巢癌组织和细胞中miR⁃216a表达水平;Transwell检测迁移和侵袭能力;Western blot和免疫荧光检测EMT相关蛋白表达;Western blot分析JAK2/STAT3途径相关蛋白表达。结果miR⁃216a在卵巢癌组织和细胞中的表达下调(P<0.05)。上调miR⁃216a削弱卵巢癌细胞迁移、侵袭和EMT,同时抑制JAK2/STAT3通路激活(P<0.05)。过表达JAK2可逆转上调miR⁃216a对以上指标的影响(P<0.05)。结论miR⁃216a可能通过抑制JAK2/STAT3通路抑制卵巢癌细胞的转移和EMT。

Objective To explore whether miRNA⁃216a(mir⁃216a)inhibits the metastasis and epithelial⁃mesenchymal transition(EMT)of ovarian cancer(OC)cells by regulating the Janus kinase 2(JAK2)/signal trans⁃ducer and activator of transcription 3(STAT3)pathway.Methods Detection of miR⁃216a expression levels in OC tissues and cells by qRT⁃PCR.Transwell were used to detect the ability of migration and invasion.Western blot and immunofluorescence were used to detect the expression levels of EMT⁃related proteins.The expression levels of JAK2/STAT3 pathway related proteins were analyzed by Western blot.Results The expression of miR⁃216a was down⁃regulated in OC tissues and cells(P<0.05).Up⁃regulated miR⁃216a impaired OC cell migration,invasion and EMT and simultaneously inhibited JAK2/STAT3 pathway activation(P<0.05).Overexpressed JAK2 reversed the effects of up⁃regulated miR⁃216a on the above indicators(P<0.05).Conclusion miR⁃216a may inhibit the metastasis and EMT of OC cells by suppressing JAK2/STAT3 pathway activation.