Document Detail

Malignant mammary cells acquire independence from extracellular context for regulation of estrogen receptor alpha.
MedLine Citation:
PMID:  14734499     Owner:  NLM     Status:  MEDLINE    
Interactions between luminal epithelial cells and their surrounding microenvironment govern the normal development and function of the mammary gland. Alterations of these interactions can induce abnormal intracellular signaling pathways that affect the development and progression of breast tumors. One critical component of mammary gland development, as well as breast cancer progression, is the expression of estrogen receptors. In a previous study using cultured nonmalignant mammary epithelial cells, we found that the basement membrane molecules, laminin-1 and collagen-IV, were involved in maintenance of estrogen receptor (ER) alpha expression, and that this response could be interfered with by disrupting cell-extracellular matrix adhesion. Here we use phenotypically normal mammary epithelial SCp2 cells to dissect the promoter region of the ERalpha that is involved in the selective response to basement membrane. We also analyze the alteration of this response in SCg6 cells, a malignant cell line that shares a common lineage with the SCp2 cells, to provide insight into the relative overexpression of ERalpha and the unresponsiveness to basement membrane regulation found in those malignant cells. Evidence is presented to show the relevance of the cross-talk between different signaling pathways in the constitution of a functional tissue organization and how this integration may be disrupted in the malignant phenotype.
Virginia Novaro; Derek C Radisky; Nancy E Ramos Castro; Alessandro Weisz; Mina J Bissell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Clinical cancer research : an official journal of the American Association for Cancer Research     Volume:  10     ISSN:  1078-0432     ISO Abbreviation:  Clin. Cancer Res.     Publication Date:  2004 Jan 
Date Detail:
Created Date:  2004-01-21     Completed Date:  2004-02-24     Revised Date:  2010-10-04    
Medline Journal Info:
Nlm Unique ID:  9502500     Medline TA:  Clin Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  402S-9S     Citation Subset:  IM    
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, and Dipartimento di Patologia generale, Seconda Università degli Studi di Napoli, Napoli, Italy.
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MeSH Terms
Estrogen Receptor alpha
Extracellular Matrix / metabolism
Gene Expression Regulation, Developmental*
Mammary Glands, Animal / metabolism
Mammary Neoplasms, Animal / metabolism,  therapy
Mice, Inbred BALB C
Models, Genetic
Promoter Regions, Genetic
Receptors, Estrogen / metabolism*
Signal Transduction
Time Factors
Transcription, Genetic
Grant Support
CA57621/CA/NCI NIH HHS; R01 CA057621-07/CA/NCI NIH HHS
Reg. No./Substance:
0/Estrogen Receptor alpha; 0/Receptors, Estrogen

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