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MicroRNA‐137 is negatively associated with clinical outcome and regulates tumor development through EZH2 in cervical cancer

We intend to evaluate the expression, clinical relevance, and functional role of microRNA‐137 (miR‐137) in human cervical cancer (CC). MiR‐137 expressions were assessed by qPCR in CC cell lines and human CC tumors. The correlation between endogenous miR‐137 expression and CC patients’ postoperative overall survival was examined statistically. CC cell lines, Ca‐Ski, and SiHa cells were transduced with lentivirus to ectopically upregulate endogenous miR‐137 expressions. Possible inhibitory effects of miR‐137 upregulation on CC in vitro proliferation and migration, as well as in vivo transplantation were evaluated. Targeting of enhancer of zeste homolog 2 (EZH2) gene by miR‐137 in CC was assessed by dual‐luciferase activity assay and qPCR. In CC cells with upregulated miR‐137, EZH2 was overexpressed to assess its direct function in miR‐137 mediated CC proliferation and migration. MiR‐137 was downregulated in both CC cells and human CC tumors. Downregulation of endogenous miR‐137 was significantly correlated with CC patients’ short overall survival. In CC cells, miR‐137 upregulation is tumor‐suppressive by inhibiting proliferation and migration in vitro, and transplantation in vivo. EZH2 was a direct downstream target gene of miR‐137 in CC. Forced overexpression of EZH2 in miR‐137‐upregulated CC cells reversed the tumor‐suppression induced by miR‐137. MiR‐137 is lowly expressed in CC and possibly acting as a negative biomarker for CC patients’ clinical outcome. MiR‐137 upregulation may suppress CC, very likely by inversely regulating EZH2.