CDCA5 is negatively regulated by miR-326 and boosts ovarian cancer progression.

PURPOSE: Ovarian cancer (OC) is the fifth leading cause of cancer death in women and one of the most prevalent malignancies in humans. Therefore, improved methods for OC early detection are urgently needed. Research has demonstrated that microRNAs (miRs) are strongly linked to OC tumorigenesis. The potential regulatory mechanism regarding miR-326 in OC is undefined. The present study was aimed to explore miR-326 expression in OC and its roles in OC progression.

METHODS

Qualitative (q)RT-PCR was adopted to examine miR-326 expression in OC tissues and cell lines in clinical samples. qRT-PCR and Western blot were applied to detect division cell cycle associated 5 (CDCA5) expression at the messenger RNA (mRNA) and protein levels. CCK-8 and Transwell invasive experiments were utilized to examine cell proliferation and invasion. Cell cycle and apoptosis were analyzed by flow cytometry. Online bioinformatics analysis was employed to predict the target genes of miR-326 and luciferase reporter genes were applied for validation.

RESULTS

MiR-326 was remarkably down-regulated in OC tissues and cell lines relative to the corresponding adjacent normal tissues and normal human ovarian surface epithelial cells (HOSE). MiR-326 overexpression markedly restrained the proliferation and invasion of OC cells, whereas miR-326 inhibitors exerted the contrary effect. Additionally, miR-326 up-regulation in OC cells prevented cells from entering S-phase and enhanced apoptosis, a phenomenon that may be due to CDCA5 down-regulation. Furthermore, we proved that CDCA5 was a downstream target of miR-326.

CONCLUSIONS

MiR-326 represses the proliferation and invasion of OC cells and enhances apoptosis by specifically modulating CDCA5 expression.