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Expression of prostate-specific antigen is transcriptionally regulated by genistein in prostate cancer cells

dc.contributor.authorDavis, Joanne N.en_US
dc.contributor.authorKucuk, Omeren_US
dc.contributor.authorSarkar, Fazlul H.en_US
dc.date.accessioned2006-04-19T14:07:17Z
dc.date.available2006-04-19T14:07:17Z
dc.date.issued2002en_US
dc.identifier.citationDavis, Joanne N.; Kucuk, Omer; Sarkar, Fazlul H. (2002)."Expression of prostate-specific antigen is transcriptionally regulated by genistein in prostate cancer cells." Molecular Carcinogenesis 34(2): 91-101. <http://hdl.handle.net/2027.42/35062>en_US
dc.identifier.issn0899-1987en_US
dc.identifier.issn1098-2744en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/35062
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12112315&dopt=citationen_US
dc.description.abstractProstate cancer is the second-leading cause of cancer-related deaths in men in the United States. Unfortunately, there is no effective therapy when prostate cancer becomes metastatic and refractory to conventional treatments. For this reason, the identification and exploration of new agents that reduce prostate cancer cell growth are of paramount importance. High consumption of plant-derived phytoestrogens is inversely associated with the incidence and mortality rate of prostate cancer. Previous studies, including our own, have shown that the phytoestrogen genistein inhibits prostate cancer cell growth in vitro and in vivo and decreases secreted and intracellular levels of the androgen-regulated protein prostate-specific antigen (PSA), but the role of genistein as an agonist/antagonist for hormone receptors remains unclear. To elucidate the mechanism by which genistein modulates PSA protein expression in prostate cancer cells, we investigated the effects of genistein on androgen-mediated and estrogen-mediated transcriptional regulation of PSA, androgen receptor (AR) mRNA and protein expression, and the ability of nuclear proteins to bind to androgen-response elements (AREs) in LNCaP cells. We showed that genistein decreased the transcriptional activation of PSA by both androgen-dependent and androgen-independent methods in LNCaP cells. The reduction of androgen-mediated transcriptional activation of PSA was correlated with decreased AR protein and mRNA levels and decreased binding to AREs. In contrast, genistein had differential effects on 17Β-estradiol–mediated PSA expressions. Low concentrations of genistein enhanced 17Β-estradiol–mediated PSA expressions, whereas high concentrations of genistein inhibited estrogen-mediated PSA expression in LNCaP cells. Genistein did not inhibit AR protein expression in the presence of 17Β-estradiol. These results suggest that ligand-dependent differences in the ability to activate PSA expression may contribute to the agonistic/antagonistic responses observed with genistein in prostate cancer cells. © 2002 Wiley-Liss, Inc.en_US
dc.format.extent268217 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherCancer Research, Oncology and Pathologyen_US
dc.titleExpression of prostate-specific antigen is transcriptionally regulated by genistein in prostate cancer cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbsecondlevelOncology and Hematologyen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Urology, University of Michigan Medical Center, Ann Arbor, Michiganen_US
dc.contributor.affiliationotherDepartment of Internal Medicine, Karmanos Cancer Institute, Wayne State University, Detroit, Michiganen_US
dc.contributor.affiliationotherDepartment of Pathology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan ; Department of Pathology, 715 Hudson Webber Cancer Center, 110 E. Warren Detroit, MI 48202.en_US
dc.identifier.pmid12112315en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/35062/1/10053_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/mc.10053en_US
dc.identifier.sourceMolecular Carcinogenesisen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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