BUB1B, negatively regulated by miR-486-5p, enhances the proliferation, migration and invasion of ovarian cancer cells

BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) belongs to the spindle assembly checkpoint protein family and is linked to the pathogenesis of diverse human cancers. This work intends to probe its expression, function and underlying molecular mechanism in ovarian cancer (OC). In the present work, gene expression profiles of GSE14407, GSE18520, and GSE54388 were obtained from the GEO database and screened for differentially expressed genes (DEGs) in ovarian cancer tissues. KM-plotter database was employed to analyze the relationship between BUB1B expression and the prognosis of OC patients. Immunohistochemistry was utilized to examine BUB1B expression in OC tissues and adjacent ovarian tissues. BUB1B expression level in OC cells was also examined using qRT-PCR. The relationship between BUB1B expression and clinicopathological parameters in OC patients was analyzed using the Chi-squared test. CCK-8 and BrdU experiments were employed to examine cell proliferation. Cell migration and invasion were detected by Transwell experiment. Western blot, qRT-PCR and dual-luciferase reporter gene analyses were employed to validate the regulatory relationship between miR-486-5p and BUB1B. In this work, we demonstrated that BUB1B was remarkably overexpressed in OC specimens compared with adjacent nontumor tissue, which was associated with higher FIGO stage and differentiation status of the patients. OC cell proliferation, migration and invasion were substantially enhanced by BUB1B overexpression; conversely, knocking down BUB1B worked the opposite effect. Mechanistically, BUB1B was one of the downstream targets of miR-486-5p and was negatively modulated by the latter. It was concluded that,BUB1B, negatively regulated by miR-486-5p, facilitates OC progression, which is a promising target for OC therapy.

Automated summary

In ovarian cancer, BUB1B, negatively regulated by miR-486-5p, promotes the progression of OC and holds promise as a therapeutic target.