Ovarian cancer is the most fatal gynecological cancer worldwide, yet the fundamental mechanism of malignancy acquisition in ovarian cancer remains unknown. miRNA has been implicated to a variety of diseases, including cancer initiation and progression. Cyclin-D2 (CCND2) is ubiquitously implicated in cancer uncontrol cell proliferation. Bioinformatic research revealed that CCND2 is a candidate gene for miR-93-5p with a binding site in its 3′UTR region in the current study. Using our ovarian cancer sample, we verified that miR-93-5p is negatively correlated with CCND2 mRNA and protein levels. Luciferase report assay revealed miR-93-5p inhibits CCND2 production through binding to the 3′UTR region. The expression of miR-93-5p in ovarian cancer patient samples was then determined, and a survival analysis was performed. Our findings showed that miR-93-5p is downregulated in ovarian cancer and is a favorable predictive factor in ovarian cancer patient. CCK8 assay, wound healing assay and flow cytometry-based cell cycle and apoptotic cell analyses were employed here. We found that miR-93-5p suppresses ovarian cancer cell proliferation and migration while enhances cell death. Our research certified that miR-93-5p reduces ovarian cancer malignancy by targeting CCND2.

Ovarian cancer is the most lethal gynecological cancer worldwide, but the underlying mechanism of ovarian cancer malignancy acquirement is largely unknown. miRNA is ubiquitously implicated in disease especially in cancer initiation and progression. In current study, we firstly detected the expression level of miR-93-5p in ovarian cancer patient samples and conducted a survival analysis. Our data revealed miR-93-5p is a favorable prognostic factor but is downregulated in ovarian cancer patients. Secondly, CCK8 assay wound healing assay and flow cytometry-based cell cycle analysis and apoptotic cell analysis were performed respectively to study the function of miR-93-5p. Functional analysis show miR-93-5p promotes ovarian cancer malignancy in term of cell proliferation, migration but reduce cell death. Bioinformatic analysis showed Cyclin-D2(CCND2) is a candidate gene of miR-93-5p with the binding site in its 3’UTR region. Furthermore, quantitive-PCR and western blot were utilized to measure miR-93-5p, CCND2 levels in tissues samples and cell lines. Our data suggested miR-93-5p is negatively correlated to the level of CCND2 mRNA and protein. Finally, Luciferase report assay was conducted, and we demonstrated miR-93-5p reduces CCND2 expression by binding to the 3’UTR region. Our study revealed the function of miR-93-5p in ovarian cancer malignancy and declaimed CCND2 as a target of miR-93-5p.