miR 488* inhibits androgen receptor expression in prostate carcinoma cells

✍ Scribed by Kavleen Sikand; Jinani E. Slaibi; Rajesh Singh; Stephen D. Slane; Girish C. Shukla

• Book ID: 102271045
• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: French
• Weight: 375 KB
• Volume: 129
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.25753

✦ Synopsis

Abstract

Androgen receptor (AR) is a ligand‐dependent transcription factor, which plays a significant role in prostate carcinogenesis. Blockade of AR and its ligand, androgen is the basis for the treatment of prostate cancer (PCa). Nevertheless, a modest increase in the critical levels of AR mRNA and corresponding protein is sufficient for the development of resistance to antiandrogen therapy. A strategy to further downregulate AR mRNA and protein expression in combination with antiandrogen therapy may prevent or delay the development of androgen‐independent PCa. Recent studies show that microRNAs (miRNAs) perform tumor suppressor functions in various cancers. In this study, we demonstrate that the overexpression of miR 488* downregulates the transcriptional activity of AR and inhibits the endogenous AR protein production in both androgen‐dependent and androgen‐independent PCa cells. In addition, miR 488* blocks the proliferation and enhances the apoptosis of PCa cells. Our data indicate that miR 488* targets AR and is a potential modulator of AR mediated signaling. Our findings provide insight for utilizing miRNAs as novel therapeutics to target AR in PCa.