Show simple item record

dc.contributor.authorMak, Paul
dc.contributor.authorLi, Jianrong
dc.contributor.authorSamanta, Sanjoy
dc.contributor.authorChang, Cheng
dc.contributor.authorJerry, D. Joseph
dc.contributor.authorDavis, Roger J.
dc.contributor.authorLeav, Irwin
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:09:19.000
dc.date.accessioned2022-08-23T16:26:23Z
dc.date.available2022-08-23T16:26:23Z
dc.date.issued2015-03-31
dc.date.submitted2015-04-24
dc.identifier.citationCell Rep. 2015 Mar 31;10(12):1982-91. doi: 10.1016/j.celrep.2015.02.063. Epub 2015 Mar 26. <a href="http://dx.doi.org/10.1016/j.celrep.2015.02.063">Link to article on publisher's site</a>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2015.02.063
dc.identifier.pmid25818291
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36553
dc.description.abstractThe role of ERbeta in prostate cancer is unclear, although loss of ERbeta is associated with aggressive disease. Given that mice deficient in ERbeta do not develop prostate cancer, we hypothesized that ERbeta loss occurs as a consequence of tumorigenesis caused by other oncogenic mechanisms and that its loss is necessary for tumorigenesis. In support of this hypothesis, we found that ERbeta is targeted for repression in prostate cancer caused by PTEN deletion and that loss of ERbeta is important for tumor formation. ERbeta transcription is repressed by BMI-1, which is induced by PTEN deletion and important for prostate tumorigenesis. This finding provides a mechanism for how ERbeta expression is regulated in prostate cancer. Repression of ERbeta contributes to tumorigenesis because it enables HIF-1/VEGF signaling that sustains BMI-1 expression. These data reveal a positive feedback loop that is activated in response to PTEN loss and sustains BMI-1.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=25818291&dopt=Abstract">Link to Article in PubMed</a>
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectCells
dc.subjectHormones, Hormone Substitutes, and Hormone Antagonists
dc.titleProstate Tumorigenesis Induced by PTEN Deletion Involves Estrogen Receptor beta Repression
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume10
dc.source.issue12
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1004&amp;context=mccb_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/mccb_pubs/5
dc.identifier.contextkey7027650
refterms.dateFOA2022-08-23T16:26:23Z
html.description.abstract<p>The role of ERbeta in prostate cancer is unclear, although loss of ERbeta is associated with aggressive disease. Given that mice deficient in ERbeta do not develop prostate cancer, we hypothesized that ERbeta loss occurs as a consequence of tumorigenesis caused by other oncogenic mechanisms and that its loss is necessary for tumorigenesis. In support of this hypothesis, we found that ERbeta is targeted for repression in prostate cancer caused by PTEN deletion and that loss of ERbeta is important for tumor formation. ERbeta transcription is repressed by BMI-1, which is induced by PTEN deletion and important for prostate tumorigenesis. This finding provides a mechanism for how ERbeta expression is regulated in prostate cancer. Repression of ERbeta contributes to tumorigenesis because it enables HIF-1/VEGF signaling that sustains BMI-1 expression. These data reveal a positive feedback loop that is activated in response to PTEN loss and sustains BMI-1.</p>
dc.identifier.submissionpathmccb_pubs/5
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages1982-91


Files in this item

Thumbnail
Name:
Publisher version
Thumbnail
Name:
journal.cellreport.10.1016.pdf
Size:
3.835Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

http://creativecommons.org/licenses/by-nc-nd/4.0/
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-nd/4.0/