Upregulation of circular RNA circ‑FAM53B predicts adverse prognosis and accelerates the progression of ovarian cancer via the miR‑646/VAMP2 and miR‑647/MDM2 signaling pathways.

Ovarian cancer (OC) is a common cancer of the human genital system. Circular RNAs (circRNAs) play an important role in carcinogenesis and progression of various cancers. The present study aimed to clarify the expression profile and functions of circ‑FAM53B in the progression of OC and reveal its underlying mechanisms. Relative levels of circ‑FAM53B in OC specimens and cell lines were determined by quantitative real‑time polymerase chain reaction (qRT‑PCR). The clinical significance of circ‑FAM53B in OC patients was analyzed through Fisher's exact test, Kaplan‑Meier curves, and Cox regression analysis. Subsequently, the regulatory effects of circ‑FAM53B on the proliferative, apoptotic, migratory, and invasive potential of OC cells were determined by loss/gain‑of‑function experiments. Mechanistically, bioinformatics analysis and luciferase reporter gene assay were used to reveal the potential molecular mechanisms of circ‑FAM53B in OC. circ‑FAM53B was overexpressed in OC specimens and cells and correlated with clinical severity and poor prognosis of OC patients. The overexpression of circ‑FAM53B accelerated the proliferation, migration, and invasion of HO8910 cells; however, it decreased the number of apoptotic cells. Silencing of circ‑FAM53B induced the opposite effect. Through dual‑luciferase reporter gene assay and functional experiments, the potential functions of circ‑FAM53B/miRNA‑646/vesicle‑associated membrane protein 2 (VAMP2) and circ‑FAM53B/miRNA‑647/mouse double minute 2 (MDM2) in mediating the progression of OC were identified. Collectively, the present results indicated that circ‑FAM53B could be a competing endogenous RNA (ceRNA) to competitively sponge miR‑646 and miR‑647 to upregulate VAMP2 and MDM2 expression at the post‑transcriptional level, thus mediating the cellular behaviors of OC cells.