Vol. 43 (x): 2017 May 5.[Ahead of print]
Zhi-Gang Yang 1, Xu-Dong Ma 1, Zhao-Hui He 2, Ying-xin Guo 1
1 Department of Urology, Baotou Central Hospital, Inner Mongolia Medical University, China; 2 Department of Urology, The First Affiliated Hospital of Guangzhou Medical University, China
Objective: miR-483-5p has been identified as a miRNA oncogene in certain cancers. However, its role in prostate cancer has not been sufficiently investigated. In this study, we investigated the role of miR-483-5p in prostate cancer and examined RBM5 regulation by miR-483-5p.
Material and methods: Expression levels of miR-483-5p were determined by quantitative real-time PCR. The effect of miR-483-5p on proliferation was evaluated by MTT assay, cell invasion was evaluated by trans-well invasion assays, and target protein expression was determined by western blotting in LNCaP, DU-145, and PC-3 cells. Luciferase reporter plasmids were constructed to confirm the action of miR-483-5p on downstream target gene RBM5 in HEK-293T cells.
Results: we observed that miR-483-5p was upregulated in prostate cancer cell lines and tissues. A miR-483-5p inhibitor inhibited prostate cancer cell growth and invasion in DU-145 and PC-3 cells. miR-483-5p directly bound to the 3’ untranslated region (3’UTR) of RBM5 in HEK-293T cells. RBM5 overexpression inhibited prostate cancer cell growth and invasion in LNCaP cells. Enforced RBM5 expression alleviated miR- 483-5p promotion of prostate cancer cell growth and invasion in LNCaP cells.
Conclusion: The present study describes a potential mechanism underlying a miR-483- 5p/RBM5 link that contributes to prostate cancer development.
Keywords: MIRN483 microRNA, human [Supplementary Concept]; RBM5 protein, human [Supplementary Concept]; Prostatic Neoplasms; Growth