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dc.contributor.authorMak, Paul
dc.contributor.authorLeav, Irwin
dc.contributor.authorPursell, Bryan M.
dc.contributor.authorBae, Donggoo
dc.contributor.authorYang, Xiaofang
dc.contributor.authorTaglienti, Cherie A.
dc.contributor.authorGouvin, Lindsey M.
dc.contributor.authorSharma, Vishva Mitra
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:39:53Z
dc.date.available2022-08-23T15:39:53Z
dc.date.issued2010-04-14
dc.date.submitted2010-11-07
dc.identifier.citationCancer Cell. 2010 Apr 13;17(4):319-32. <a href="http://dx.doi.org/10.1016/j.ccr.2010.02.030">Link to article on publisher's site</a>
dc.identifier.issn1535-6108 (Linking)
dc.identifier.doi10.1016/j.ccr.2010.02.030
dc.identifier.pmid20385358
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26278
dc.description.abstractHigh Gleason grade prostate carcinomas are aggressive, poorly differentiated tumors that exhibit diminished estrogen receptor beta (ERbeta) expression. We report that a key function of ERbeta and its specific ligand 5alpha-androstane-3beta,17beta-diol (3beta-adiol) is to maintain an epithelial phenotype and repress mesenchymal characteristics in prostate carcinoma. Stimuli (TGF-beta and hypoxia) that induce an epithelial-mesenchymal transition (EMT) diminish ERbeta expression, and loss of ERbeta is sufficient to promote an EMT. The mechanism involves ERbeta-mediated destabilization of HIF-1alpha and transcriptional repression of VEGF-A. The VEGF-A receptor neuropilin-1 drives the EMT by promoting Snail1 nuclear localization. Importantly, this mechanism is manifested in high Gleason grade cancers, which exhibit significantly more HIF-1alpha and VEGF expression, and Snail1 nuclear localization compared to low Gleason grade cancers.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20385358&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.ccr.2010.02.030
dc.subjectEpithelial Cells
dc.subjectEstrogen Receptor beta
dc.subjectHumans
dc.subjectHypoxia-Inducible Factor 1, alpha Subunit
dc.subjectMale
dc.subjectMesoderm
dc.subjectProstatic Neoplasms
dc.subjectTranscription Factors
dc.subjectTransforming Growth Factor beta
dc.subjectVascular Endothelial Growth Factor A
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleERbeta impedes prostate cancer EMT by destabilizing HIF-1alpha and inhibiting VEGF-mediated snail nuclear localization: implications for Gleason grading
dc.typeJournal Article
dc.source.journaltitleCancer cell
dc.source.volume17
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/192
dc.identifier.contextkey1633418
html.description.abstract<p>High Gleason grade prostate carcinomas are aggressive, poorly differentiated tumors that exhibit diminished estrogen receptor beta (ERbeta) expression. We report that a key function of ERbeta and its specific ligand 5alpha-androstane-3beta,17beta-diol (3beta-adiol) is to maintain an epithelial phenotype and repress mesenchymal characteristics in prostate carcinoma. Stimuli (TGF-beta and hypoxia) that induce an epithelial-mesenchymal transition (EMT) diminish ERbeta expression, and loss of ERbeta is sufficient to promote an EMT. The mechanism involves ERbeta-mediated destabilization of HIF-1alpha and transcriptional repression of VEGF-A. The VEGF-A receptor neuropilin-1 drives the EMT by promoting Snail1 nuclear localization. Importantly, this mechanism is manifested in high Gleason grade cancers, which exhibit significantly more HIF-1alpha and VEGF expression, and Snail1 nuclear localization compared to low Gleason grade cancers.</p>
dc.identifier.submissionpathcancerbiology_pp/192
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages319-32


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