Document Detail


RelB NF-kappaB represses estrogen receptor alpha expression via induction of the zinc finger protein Blimp1.
MedLine Citation:
PMID:  19433448     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aberrant constitutive expression of NF-kappaB subunits, reported in more than 90% of breast cancers and multiple other malignancies, plays pivotal roles in tumorigenesis. Higher RelB subunit expression was demonstrated in estrogen receptor alpha (ERalpha)-negative breast cancers versus ERalpha-positive ones, due in part to repression of RelB synthesis by ERalpha signaling. Notably, RelB promoted a more invasive phenotype in ERalpha-negative cancers via induction of the BCL2 gene. We report here that RelB reciprocally inhibits ERalpha synthesis in breast cancer cells, which contributes to a more migratory phenotype. Specifically, RelB is shown for the first time to induce expression of the zinc finger repressor protein Blimp1 (B-lymphocyte-induced maturation protein), the critical mediator of B- and T-cell development, which is transcribed from the PRDM1 gene. Blimp1 protein repressed ERalpha (ESR1) gene transcription. Commensurately higher Blimp1/PRDM1 expression was detected in ERalpha-negative breast cancer cells and primary breast tumors. Induction of PRDM1 gene expression was mediated by interaction of Bcl-2, localized in the mitochondria, with Ras. Thus, the induction of Blimp1 represents a novel mechanism whereby the RelB NF-kappaB subunit mediates repression, specifically of ERalpha, thereby promoting a more migratory phenotype.
Authors:
Xiaobo Wang; Karine Belguise; Christine F O'Neill; Nuria Sánchez-Morgan; Mathilde Romagnoli; Sean F Eddy; Nora D Mineva; Ziyang Yu; Chengyin Min; Vickery Trinkaus-Randall; Dany Chalbos; Gail E Sonenshein
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-05-11
Journal Detail:
Title:  Molecular and cellular biology     Volume:  29     ISSN:  1098-5549     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-29     Completed Date:  2009-07-13     Revised Date:  2014-04-21    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3832-44     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Base Sequence
Breast Neoplasms / genetics,  metabolism
Cell Line, Tumor
Cell Movement
DNA Primers / genetics
Estrogen Receptor alpha / genetics,  metabolism*
Female
Gene Expression
Genes, bcl-2
Humans
Neoplasms, Hormone-Dependent / genetics,  metabolism
Phenotype
Proto-Oncogene Proteins c-bcl-2 / metabolism
Repressor Proteins / biosynthesis*,  genetics,  metabolism
Transcription Factor RelB / metabolism*
ras Proteins / metabolism
Grant Support
ID/Acronym/Agency:
P01 ES011624/ES/NIEHS NIH HHS; P01 ES11624/ES/NIEHS NIH HHS; R01 CA036355/CA/NCI NIH HHS; R01 CA129129/CA/NCI NIH HHS; R01 CA129129/CA/NCI NIH HHS; R01 CA36355/CA/NCI NIH HHS; R01 EY006000-25/EY/NEI NIH HHS; R01 EY06000/EY/NEI NIH HHS; T32 HL007501/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/DNA Primers; 0/Estrogen Receptor alpha; 0/Proto-Oncogene Proteins c-bcl-2; 0/RELB protein, human; 0/Repressor Proteins; 138415-26-6/PRDM1 protein, human; 147337-75-5/Transcription Factor RelB; EC 3.6.5.2/ras Proteins
Comments/Corrections

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


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