期刊
INTERNATIONAL JOURNAL OF CANCER
卷 129, 期 4, 页码 810-819出版社
WILEY
DOI: 10.1002/ijc.25753
关键词
androgen receptor; miRNA; prostate cancer
类别
资金
- CDMRP [W81XWH-06-1-0191]
- NSF
- BCRP
- PCRP of CDMRP/DoD
- Board of Regents, Ohio
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.
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