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• W2138885835 startingPage "5175" @default.
• W2138885835 abstract "Androgen receptor (AR) overexpression is one of the characteristics of prostate cancer (PC) that progresses to hormone independence. An androgen-independent (AI) derivative, with much higher AR-mRNA and protein levels than the parental LNCaP cell line, whose proliferation was androgen dependent (AD), was used to explore the mechanism of AR overexpression. We found that a suppressor element (ARS), previously identified in mouse AR and located in the 5′-untranslated region of human AR gene, malfunctions in AI cells. Transfection of constructs that included ARS element into AD cells reduced the transactivating activities of both AR promoter and a heterologous SV40 promoter. The deletion of ARS resulted in an eightfold increase in AR-promoter activity in AD cells, but had no effect in AI cells. Moreover, the nuclear extracts of AD cells contained proteins that produced a specific, ARS-binding complex, while this complex appeared to have been lost from AI cells. Most importantly, treatment of AI cells with a demethylating agent or histone deacetylase inhibitors restored the lost ARS-binding complex. The restoration of the complex coincided with a reduced expression of AR-mRNA and protein and a reduced rate of AR-gene transcription, determined by nuclear run-on experiment. Thus, epigenetic transcriptional silencing of the suppressor protein(s) may be responsible for AR overexpression in AI cells, and its reversal in hormone-independent PC may normalize AR levels and restore their hormone dependence." @default.
• W2138885835 created "2016-06-24" @default.
• W2138885835 creator A5035980413 @default.
• W2138885835 creator A5041082380 @default.
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• W2138885835 date "2004-05-24" @default.
• W2138885835 modified "2023-10-18" @default.
• W2138885835 title "Androgen receptor level controlled by a suppressor complex lost in an androgen-independent prostate cancer cell line" @default.
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• W2138885835 doi "https://doi.org/10.1038/sj.onc.1207654" @default.
• W2138885835 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15156193" @default.
• W2138885835 hasPublicationYear "2004" @default.
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