microRNA-503 suppresses the migration, proliferation and colony formation of prostate cancer cells by targeting tumor protein D52 like 2
- Yuhua Chi
- Feng Ding
- Wenjie Zhang
- Lifa Du
Published online on: October 30, 2017
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.