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The estrogen-dependent c-JunER protein causes a reversible loss of mammary epithelial cell polarity involving a destabilization of adherens junctions.
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MedLine Citation:
PMID:  8601589     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Members of the epidermal growth factor (EGF) receptor family are known to be specifically involved in mammary carcinogenesis. As a nuclear target of activated receptors, we examined c-Jun in mammary epithelial cells. For this, we used a c-JunER fusion protein which was tightly controlled by estrogen. Activation of the JunER by hormone resulted in the transcriptional regulation of a variety of AP-1 target genes. Hormone-activated JunER induced the loss of epithelial polarity, a disruption of intercellular junctions and normal barrier function and the formation of irregular multilayers. These changes were completely reversible upon hormone withdrawal. Loss of epithelial polarity involved redistribution of both apical and basolateral proteins to the entire plasma membrane. The redistribution of E-cadherin and beta-catenin was accompanied by a destabilization of complexes formed between these two proteins, leading to an enrichment of beta-catenin in the detergent-soluble fraction. Uninduced cells were able to form three-dimensional tubular structures in collagen I gels which were disrupted upon JunER activation, leading to irregular cell aggregates. The JunER-induced disruption of tubular structures was dependent on active signaling by growth factors. Moreover, the effects of JunER could be mimicked in normal cells by the addition of acidic fibroblast growth factor (aFGF). These data suggest that a possible function of c-Jun in epithelial cells is to modulate epithelial polarity and regulate tissue organization, processes which may be equally important for both normal breast development and as initiating steps in carcinogenesis.
Authors:
I Fialka; H Schwarz; E Reichmann; M Oft; M Busslinger; H Beug
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of cell biology     Volume:  132     ISSN:  0021-9525     ISO Abbreviation:  J. Cell Biol.     Publication Date:  1996 Mar 
Date Detail:
Created Date:  1996-05-09     Completed Date:  1996-05-09     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0375356     Medline TA:  J Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1115-32     Citation Subset:  IM    
Affiliation:
Research Institute of Molecular Pathology, Vienna, Austria.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cadherins / metabolism
Cell Adhesion
Cell Line, Transformed
Cell Polarity*
Collagen
Cytoskeletal Proteins / metabolism
Epithelial Cells
Epithelium / drug effects
Estradiol / pharmacology*
Female
Gels
Gene Expression Regulation / drug effects*
Growth Substances / pharmacology
Intercellular Junctions / ultrastructure*
Mammary Glands, Animal / cytology*,  drug effects
Membrane Proteins / metabolism
Mice
Phosphorylation
Protein Processing, Post-Translational
Proto-Oncogene Proteins c-jun / genetics,  physiology*
Receptors, Estrogen / genetics,  physiology*
Recombinant Fusion Proteins / metabolism*
Trans-Activators*
Transcription Factor AP-1 / physiology
Transfection
beta Catenin
Chemical
Reg. No./Substance:
0/Cadherins; 0/Catnb protein, mouse; 0/Cytoskeletal Proteins; 0/Gels; 0/Growth Substances; 0/Membrane Proteins; 0/Proto-Oncogene Proteins c-jun; 0/Receptors, Estrogen; 0/Recombinant Fusion Proteins; 0/Trans-Activators; 0/Transcription Factor AP-1; 0/beta Catenin; 50-28-2/Estradiol; 9007-34-5/Collagen
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): J Cell Biol
ISSN: 0021-9525
ISSN: 1540-8140
Publisher: The Rockefeller University Press
Article Information
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Print publication date: Day: 2 Month: 3 Year: 1996
Volume: 132 Issue: 6
First Page: 1115 Last Page: 1132
ID: 2120757
Publisher Id: 96176306
PubMed Id: 8601589

The estrogen-dependent c-JunER protein causes a reversible loss of mammary epithelial cell polarity involving a destabilization of adherens junctions


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