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• W2114588554 abstract "Abstract The androgen receptor (AR) is critical in the normal development and function of the prostate, as well as in prostate carcinogenesis. Androgen deprivation therapy is the mainstay in the treatment of advanced prostate cancer; however, after an initial response, the disease inevitably progresses to castration-resistant prostate cancer (CRPC). Recent evidence suggests that continued AR activation, sometimes in a ligand-independent manner, is commonly associated with the development of CRPC. Thus, novel agents targeting the AR are urgently needed as a strategic step in developing new therapies for this disease state. In this study, we investigated the effect of berberine on AR signaling in prostate cancer. We report that berberine decreased the transcriptional activity of AR. Berberine did not affect AR mRNA expression, but induced AR protein degradation. Several ligand-binding, domain-truncated AR splice variants have been identified, and these variants are believed to promote the development of CRPC in patients. Interestingly, we found that these variants were more susceptible to berberine-induced degradation than the full-length AR. Furthermore, although the growth of LNCaP xenografts in nude mice was inhibited by berberine, and AR expression was reduced in the tumors, the morphology and AR expression in normal prostates were not affected. This study is the first to show that berberine suppresses AR signaling and suggests that berberine, or its derivatives, presents a promising agent for the prevention and/or treatment of prostate cancer. Mol Cancer Ther; 10(8); 1346–56. ©2011 AACR." @default.
• W2114588554 created "2016-06-24" @default.
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• W2114588554 date "2011-08-01" @default.
• W2114588554 modified "2023-10-14" @default.
• W2114588554 title "Berberine Suppresses Androgen Receptor Signaling in Prostate Cancer" @default.
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• W2114588554 doi "https://doi.org/10.1158/1535-7163.mct-10-0985" @default.
• W2114588554 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3154574" @default.
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