Circ-UBAP2 functions as sponges of miR-1205 and miR-382 to promote glioma progression by modulating STC1 expression.

Abstract

BackgroundCircular RNAs (circRNAs) exert vital functions in glioma pathogenesis. CircRNA ubiquitin‐associated protein 2 (circ‐UBAP2, hsa_circ_0008344) has been illuminated as a tumor driver in glioma. Nevertheless, the mechanisms underlying the oncogenic regulation of circ‐UBAP2 in glioma are still undefined.MethodsCirc‐UBAP2, miR‐1205, miR‐382, and GPRC5A were quantified using qRT‐PCR and western blot. Cell viability was detected using a CCK‐8 assay. Cell migration and invasion were measured using the would‐healing and transwell assays. Flow cytometry and colony formation assay were applied to evaluate cell apoptosis and colony formation, respectively. The xenograft model assays were used to examine the impact of circ‐UBAP2 on tumorigenic effect in vivo. Direct relationships among circ‐UBAP2, miR‐1205, miR‐382, and GPRC5A were confirmed using dual‐luciferase reporter assays.ResultsCirc‐UBAP2 expression was upregulated in glioma. The reduced level of circ‐UBAP2 hampered cell proliferation, migration, invasion, and enhanced apoptosis in vitro and weakened tumor growth in vivo. Mechanistically, circ‐UBAP2 directly bound to miR‐1205 and miR‐382. miR‐1205 and miR‐382 mediated the regulation of circ‐UBAP2 silencing on glioma cell behaviors. Moreover, GPRC5A was a functional target of miR‐1205 and miR‐382 in regulating glioma cell behaviors. Furthermore, circ‐UBAP2 mediated GPRC5A expression through miR‐1205 or miR‐382 in glioma cells.ConclusionOur current findings identified that circ‐UBAP2 silencing impeded glioma malignant progression partially by downregulating GPRC5A through targeting miR‐1205 and miR‐382.