MicroRNAs (miRNAs) are small regulatory non-coding RNAs that have been reported to play an important role in the tumorigenesis of many cancers. In addition, miRNAs might serve as new promising biomarkers for diagnosis and prognosis and as effective therapeutic targets for patients with such malignancies. Accordingly, the dysregulation of miR-212-3p has been reported in a variety of human cancers. However, its biological functions and molecular mechanisms high-grade serous ovarian cancer (HGSOG) remain unknown. In this study, we demonstrated that miR-212-3p interacts with MAP3K3 based on bioinformatics-based predictions. Further, MAP3K3 was identified as a direct target gene of miR-212-3p in HGSOC. In addition, overexpression of miR-212-3p in HGSOC inhibited cell proliferation, colony formation, invasion, and migration. In contrast MAP3K3 mitigated the suppressive effects of miR-212-3p on HGSOC cell proliferation, invasion, and migration. Furthermore, miR-212-3p was significantly downregulated in HGSOC tissues compared to expression in normal fallopian tube tissues and was inversely associated with MAP3K3 levels. Accordingly, low miR-212-3p expression was also correlated with poor prognosis for HGSOC patients. In conclusion, miR-212-3p might act as a suppressor of HGSOC carcinogenesis by directly targeting MAP3K3. Therefore, this miRNA could be a novel and effective target for the treatment of patients with HGSOC.
Keywords: MAP3K3; high-grade serous ovarian cancer (HGSOC); miR-212-3p; tumor suppressor.
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