Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Estrogen Receptor beta 2 Induces Hypoxia Signature of Gene Expression by Stabilizing HIF-1 alpha in Prostate Cancer
Show others and affiliations
2015 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, no 5, e0128239Article in journal (Refereed) Published
Abstract [en]

The estrogen receptor (ER) beta variant ER beta 2 is expressed in aggressive castration-resistant prostate cancer and has been shown to correlate with decreased overall survival. Genome-wide expression analysis after ER beta 2 expression in prostate cancer cells revealed that hypoxia was an overrepresented theme. Here we show that ER beta 2 interacts with and stabilizes HIF-1 alpha protein in normoxia, thereby inducing a hypoxic gene expression signature. HIF-1 alpha is known to stimulate metastasis by increasing expression of Twist1 and increasing vascularization by directly activating VEGF expression. We found that ER beta 2 interacts with HIF-1 alpha and piggybacks to the HIF-1 alpha response element present on the proximal Twist1 and VEGF promoters. These findings suggest that at least part of the oncogenic effects of ER beta 2 is mediated by HIF-1 alpha and that targeting of this ER beta 2 -HIF-1 alpha interaction may be a strategy to treat prostate cancer.

Place, publisher, year, edition, pages
2015. Vol. 10, no 5, e0128239
Keyword [en]
Tumor-Suppressor Protein, Hippel-Lindau Protein, Androgen Receptor, Er-Beta, Alpha, Growth, Hif, Transcription, Metastasis, Mechanism
National Category
Biological Sciences Medical and Health Sciences
Identifiers
URN: urn:nbn:se:kth:diva-169966DOI: 10.1371/journal.pone.0128239ISI: 000355183900212PubMedID: 26010887Scopus ID: 2-s2.0-84930221880OAI: oai:DiVA.org:kth-169966DiVA: diva2:826509
Funder
Swedish Cancer SocietyEU, FP7, Seventh Framework Programme, GROWTH 291795Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Note

QC 20150625

Available from: 2015-06-25 Created: 2015-06-25 Last updated: 2017-12-04Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMedScopus

Authority records BETA

Williams, Cecilia

Search in DiVA

By author/editor
Williams, Cecilia
By organisation
Proteomics and NanobiotechnologyScience for Life Laboratory, SciLifeLab
In the same journal
PLoS ONE
Biological SciencesMedical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 65 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf