MicroRNA-215 (miR-215) has been showed to play crucial roles in tumorigenesis and tumor progression in many types of cancer. However, its biological function and underlying mechanism in epithelial ovarian cancer (EOC) remains greatly unknown. The aims of this study were to investigate biological role and underlying mechanism of miR-215 in EOC. Here, we found that miR-215 expression was significantly decreased in EOC tissues or cell lines compared with adjacent normal tissues or normal ovarian cell line. Decreased miR-215 expression was significantly associated with International Federation of Gynaecology and Obstetrics (FIGO) stage and lymph node metastasis. Function analysis revealed that overexpression of miR-215 using miR-215 mimic significantly inhibit EOC cell proliferation, colony formation, migration and invasion in vitro. as well as suppress tumor growth in vivo. Moreover, we identified ribosome assembly factor NIN/RPN12 binding protein (NOB1) as a direct targets for miR-215 binding, resulting in suppression it expression, which in turn activated the MAPK signaling pathway. In clinical EOC specimens, NOB1 expression was upregulated, and inversely correlated with miR-215 expression (r = -0.675, P<0.001). Overexpression of NOB1 effectively rescued inhibition effect on EOC cells by induced miR-215 overexpression. Taken together, our findings suggested that miR-215 suppressed EOC growth and invasion by targeting NOB1.
Keywords: MicroRNAs; NOB1; epithelial ovarian cancer; miR-215.