THUMPD3‐AS1 inhibits ovarian cancer cell apoptosis through the miR‐320d/ARF1 axis

Abstract Ovarian cancer is one of the most common gynecologic malignancies that has a poor prognosis. THUMPD3‐AS1 is an oncogenic long noncoding RNA (lncRNA) in several cancers. Moreover, miR‐320d is downregulated and inhibited proliferation in ovarian cancer cells, whereas ARF1 was upregulated and promoted the malignant progression in epithelial ovarian cancer. Nevertheless, the role of THUMPD3‐AS1 in ovarian cancer and the underlying mechanism has yet to be elucidated. Human normal ovarian epithelial cells (IOSE80) and ovarian cancer cell lines (CAVO3, A2780, SKOV3, OVCAR3, and HEY) were adopted for in vitro experiments. The functional roles of THUMPD3‐AS1 in cell viability and apoptosis were determined using CCK‐8, flow cytometry, and TUNEL assays. Western blot was performed to assess the protein levels of ARF1 , Bax , Bcl‐2 , and caspase 3 , whereas RT‐qPCR was applied to measure ARF1 mRNA, THUMPD3‐AS1 , and miR‐320d levels. The targeting relationship between miR‐320d and THUMPD3‐AS1 or ARF1 was validated with dual luciferase assay. THUMPD3‐AS1 and ARF1 were highly expressed in ovarian cancer cells, whereas miR‐320d level was lowly expressed. THUMPD3‐AS1 knockdown was able to repress cell viability and accelerate apoptosis of OVCAR3 and SKOV3 cells. Also, THUMPD3‐AS1 acted as a sponge of miR‐320d , preventing the degradation of ARF1 . MiR‐320d downregulation reversed the tumor suppressive function induced by THUMPD3‐AS1 depletion. Additionally, miR‐320d overexpression inhibited ovarian cancer cell viability and accelerated apoptosis, which was overturned by overexpression of ARF1 . THUMPD3‐AS1 inhibited ovarian cancer cell apoptosis by modulation of miR‐320d / ARF1 axis. The discoveries might provide a prospective target for ovarian cancer treatment.