microRNA-503 suppresses the migration, proliferation and colony formation of prostate cancer cells by targeting tumor protein D52 like 2.

The present study investigated the expression of microRNA-503 (miR-503) and its effect and mechanism of action on prostate cancer. Tumor tissues and tumor-adjacent tissues were collected from 20 patients with prostate cancer. TargetScan was used to predict the miRNA molecule that interacts with tumor protein D52 like 2 (TPD52L2). DU145 cells were transfected with a negative control, miR-503 mimic or miR-503 inhibitor. DU145 cells that had not undergone transfection were used as a control. Levels of miR-503 and TPD52L2 mRNA were determined using reverse transcription-quantitative polymerase chain reaction and the expression of TPD52L2 protein was measured using western blot analysis. The migration ability of DU145 cells was evaluated using a Transwell assay and cell proliferation was examined using an MTT assay. A flat plate colony formation test was conducted to examine the colony formation rate of DU145 cells. The current study demonstrated that TPD52L2 expression is increased while miR-503 expression is decreased in prostate cancer tissues. Overexpression of miR-503 inhibited the transcription and translation of TPD52L2 in DU145 cells and reduced cell migration, proliferation and colony formation. By contrast, inhibition of miR-503 expression increased the expression of TPD52L2 in DU145 cells and increased cell migration, proliferation and colony formation. The present study demonstrated that miR-503 is an oncogene that regulates the migration, proliferation and colony formation of prostate cancer cells by targeting the TPD52L2 gene. Thus, miR-503 has the potential to become a target for the molecular treatment and prognosis of prostate cancer in the future.