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.