Circ_0005276 Promotes Prostate Cancer Progression Through the Crosstalk of miR-128-3p/DEPDC1B Axis

This study aimed to investigate more detailed functions of circ_0005276 in prostate cancer (PCa) and provide a novel mechanism for circ_0005276 action. The expression of circ_0005276, microRNA-128-3p (miR-128-3p) and DEP domain containing 1B (DEPDC1B) was detected by quantitative real-time PCR. In functional assays, cell proliferation was determined by CCK-8 assay and EdU assay. Cell migration and invasion were determined by transwell assay. The ability of angiogenesis was determined by tube formation assay. Cell apoptosis was determined by flow cytometry assay. The potential binding relationship between miR-128-3p and circ_0005276 or DEPDC1B was ascertained by dual-luciferase reporter assay and RIP assay. Mouse models were used to verify the role of circ_0005276 in vivo. The upregulation of circ_0005276 was determined in PCa tissues and cells. Circ_0005276 knockdown inhibited proliferation, migration, invasion and angiogenesis in PCa cells, and circ_0005276 knockdown also blocks tumor growth in vivo. Mechanism analysis discovered that miR-128-3p was a target of circ_0005276, and miR-128-3p inhibition recovered circ_0005276 knockdown-inhibited proliferation, migration, invasion and angiogenesis. In addition, DEPDC1B was a target of miR-128-3p, and miR-128-3p restoration-inhibited proliferation, migration, invasion and angiogenesis were rescued by DEPDC1B overexpression. Circ_0005276 might promote the development of PCa by activating the expression of DEPDC1B via targeting miR-128-3p.