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Int. braz. j. urol ; 43(6): 1060-1067, Nov.-Dec. 2017. graf
Article in English | LILACS | ID: biblio-892928

ABSTRACT

ABSTRACT 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.


Subject(s)
Humans , Male , Prostatic Neoplasms/genetics , Prostatic Neoplasms/pathology , Gene Expression Regulation, Neoplastic/genetics , Cell Cycle Proteins/metabolism , Untranslated Regions/genetics , Tumor Suppressor Proteins/metabolism , MicroRNAs/physiology , Cell Proliferation/genetics , DNA-Binding Proteins/metabolism , Real-Time Polymerase Chain Reaction , Prostatic Neoplasms/mortality , Down-Regulation , Up-Regulation , RNA-Binding Proteins/metabolism , MicroRNAs/antagonists & inhibitors , Cell Line, Tumor , Neoplasm Invasiveness
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