MicroRNA let-7c Suppresses Androgen Receptor Expression and Activity via Regulation of Myc Expression in Prostate Cancer Cells
Year: 2011
Type: article
Abstract: Castration-resistant prostate cancer continues to rely on androgen receptor (AR) expression. AR plays a central role in the development of prostate cancer and progression to castration resistance during and after androgen deprivation therapy. Here, we identified miR-let-7c as a key regulator of expression of AR. miR-let-7c suppresses AR expression and activity in human prostate cancer cells by targeting its transcription via c-Myc. Suppression of AR by let-7c leads to decreased cell proliferation of human prostate cancer cells. Down-regulation of Let-7c in prostate cancer specimens is inversely correlated with AR expression, whereas the expression of Lin28 (a repressor of let-7) is correlated positively with AR expression. Our study demonstrates that the miRNA let-7c plays an important role in the regulation of androgen signaling in prostate cancer by down-regulating AR expression. These results suggest that reconstitution of miR-let-7c may aid in targeting enhanced and hypersensitive AR in advanced prostate cancer.
Source: Journal of Biological Chemistry
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,430
Funder: National Cancer Institute
Awards: G2427494278, Novel roles of microRNA in androgen receptor signaling, Selenium regulates androgen receptor signaling in prostate cancer, G5746723242, The role of DNA polymerase eta in DNA damage response and p53 activation, Interleukin-6 and castration-resistant prostate cancer, IL-4 and androgen receptor signaling in prostate cancer, G6820733645, Mechanism of P73-dependent Tumor Suppression, Cancer Center Support Grant P30
OpenAlex ID: W1983675397