Mechanisms of androgen receptor repression in prostate cancer

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Campo DC	Valor	Lengua/Idioma
dc.contributor.author	Belandia, Borja	-
dc.contributor.author	Bevan, Charlotte L.	-
dc.date.accessioned	2010-05-26T11:49:34Z	-
dc.date.available	2010-05-26T11:49:34Z	-
dc.date.issued	2006-12	-
dc.identifier.citation	Biochemical Society Transactions 34(6): 1124-1127 (2006)	en_US
dc.identifier.issn	0300-5127	-
dc.identifier.uri	http://hdl.handle.net/10261/24725	-
dc.description	4 pages, 2 figures, 1 table.-- El pdf del artículo es la versión de autor.-- et al.	en_US
dc.description.abstract	Anti-androgens used in prostate cancer therapy inhibit AR (androgen receptor) activity via largely unknown mechanisms. Although initially successful in most cases, they eventually fail and the disease progresses. We need to elucidate how anti-androgens work to understand why they fail, and prolong their effects or design further therapies. Using a cellular model, we found different anti-androgens have diverse effects on subcellular localization of AR, revealing that they work via different mechanisms and suggesting that an informed sequential treatment regime may benefit patients. In the presence of the anti-androgens bicalutamide and hydroxyflutamide, a significant proportion of the AR is translocated to the nucleus but remains inactive. Receptor inhibition under these conditions is likely to involve recruitment of co-repressor proteins, which interact with antagonist-occupied receptor but inhibit receptor-dependent transcription. Which co-repressors are required in vivo for AR repression by anti-androgens is not clear, but one candidate is the Notch effector Hey1. This inhibits ligand-dependent activity of the AR but not other steroid receptors. Further, it is excluded from the nucleus in most human prostate cancers, suggesting that abnormal subcellular distribution of co-repressors may contribute to the aberrant hormonal responses observed in prostate cancer. A decrease in co-repressor function is one possible explanation for the development of anti-androgen-resistant prostate cancer, and this suggests that it may not occur at the gross level of protein expression.	en_US
dc.description.sponsorship	Studies described here were supported by grants from The Prostate Cancer Charity and the Association for International Cancer Research.	en_US
dc.format.extent	213793 bytes	-
dc.format.mimetype	application/pdf	-
dc.language.iso	eng	en_US
dc.publisher	Portland Press	en_US
dc.publisher	Biochemical Society	-
dc.rights	openAccess	en_US
dc.subject	Androgen receptor	en_US
dc.subject	Antiandrogens	en_US
dc.subject	Corepressor	en_US
dc.subject	Prostate cancer	en_US
dc.title	Mechanisms of androgen receptor repression in prostate cancer	en_US
dc.type	artículo	en_US
dc.description.peerreviewed	Peer reviewed	en_US
dc.relation.publisherversion	http://www.biochemsoctrans.org/bst/034/1124/bst0341124.htm	en_US
dc.type.coar	http://purl.org/coar/resource_type/c_6501	es_ES
item.cerifentitytype	Publications	-
item.openairecristype	http://purl.org/coar/resource_type/c_18cf	-
item.grantfulltext	open	-
item.openairetype	artículo	-
item.fulltext	With Fulltext	-
item.languageiso639-1	en	-
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