Document Detail


Pharmacological uncoupling of androgen receptor-mediated prostate cancer cell proliferation and prostate-specific antigen secretion.
MedLine Citation:
PMID:  14633736     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The androgen receptor (AR), a member of the nuclear receptor family, is a ligand-inducible transcription factor. In the prostate gland, androgens regulate the transcription of several genes that ultimately result in cell growth and differentiation. With a goal of developing tissue-selective AR modulators that can be used to treat prostate cancer and other androgenopathies, we have taken an approach to identify androgens that function in a manner distinct from the physiological androgens testosterone and dihydrotestosterone. Classical AR agonists function by binding to and inducing a conformational change in the receptor. This facilitates the obligate interaction of the amino and carboxyl terminus of the receptor, recruitment of coactivators, and subsequent regulation of target genes. On the basis of this paradigm, we screened a library of potential AR agonists for compounds that induce an "activating" conformational change in the receptor structure but that do not facilitate a high-affinity intermolecular interaction between the amino and carboxyl terminus. Compounds identified in this manner behaved as partial agonists of AR-mediated transcription in a variety of assays. Additional compounds were identified in this screen that did not allow the activation function-2 coactivator pocket to form and were demonstrated to function as weak agonists of AR-mediated transcription. Surprisingly, when we examined the ability of these compounds to induce cell proliferation, we observed that despite having different degrees of partial agonist activities on classical transcriptional responses (i.e., induction of prostate-specific antigen), these compounds were as efficacious as dihydrotestosterone in stimulating proliferation. The unexpected finding that AR-mediated transcription and proliferation can be uncoupled suggests that AR is not used in the same manner in all androgen-regulated biological processes.
Authors:
Ganesan Sathya; Ching-yi Chang; Dmitri Kazmin; C Edgar Cook; Donald P McDonnell
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  63     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-11-24     Completed Date:  2004-02-09     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8029-36     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
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MeSH Terms
Descriptor/Qualifier:
Androgens / pharmacology,  physiology
Animals
Cell Division / drug effects,  physiology
Haplorhini
Humans
Male
Prostate-Specific Antigen / secretion*
Prostatic Neoplasms / drug therapy*,  pathology,  secretion
Receptors, Androgen / agonists*,  physiology
Transcriptional Activation / drug effects,  physiology
Transfection
Grant Support
ID/Acronym/Agency:
CA 95094-02/CA/NCI NIH HHS; DK 50494/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Androgens; 0/Receptors, Androgen; EC 3.4.21.77/Prostate-Specific Antigen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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