Document Detail


Matrix density-induced mechanoregulation of breast cell phenotype, signaling and gene expression through a FAK-ERK linkage.
MedLine Citation:
PMID:  19826415     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mammographically dense breast tissue is one of the greatest risk factors for developing breast carcinoma, yet the associated molecular mechanisms remain largely unknown. Importantly, regions of high breast density are associated with increased stromal collagen and epithelial cell content. We set out to determine whether increased collagen-matrix density, in the absence of stromal cells, was sufficient to promote proliferation and invasion characteristic of a malignant phenotype in non-transformed mammary epithelial cells. We demonstrate that increased collagen-matrix density increases matrix stiffness to promote an invasive phenotype. High matrix stiffness resulted in increased formation of activated three-dimensional (3D)-matrix adhesions and a chronically elevated outside-in/inside-out focal adhesion (FA) kinase (FAK)-Rho signaling loop, which was necessary to generate and maintain the invasive phenotype. Moreover, this signaling network resulted in hyperactivation of the Ras-mitogen-activated protein kinase (MAPK) pathway, which promoted growth of mammary epithelial cells in vitro and in vivo and activated a clinically relevant proliferation signature that predicts patient outcome. Hence, the current data provide compelling evidence for the importance of the mechanical features of the microenvironment, and suggest that mechanotransduction in these cells occurs through a FAK-Rho-ERK signaling network with extracellular signal-regulated kinase (ERK) as a bottleneck through which much of the response to mechanical stimuli is regulated. As such, we propose that increased matrix stiffness explains part of the mechanism behind increased epithelial proliferation and cancer risk in human patients with high breast tissue density.
Authors:
P P Provenzano; D R Inman; K W Eliceiri; P J Keely
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  28     ISSN:  1476-5594     ISO Abbreviation:  Oncogene     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-01-05     Revised Date:  2011-08-22    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  4326-43     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Wisconsin, Madison, WI, USA. ppproven@fhcrc.org
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MeSH Terms
Descriptor/Qualifier:
Breast Neoplasms / etiology,  genetics,  metabolism
Carcinoma / etiology,  genetics,  metabolism
Cell Count
Cell Proliferation
Cell Transformation, Neoplastic / genetics,  metabolism
Cells, Cultured
Extracellular Matrix / chemistry,  physiology*
Extracellular Signal-Regulated MAP Kinases / metabolism,  physiology*
Female
Focal Adhesion Kinase 1 / metabolism,  physiology*
Gene Expression / physiology
Gene Expression Profiling
Humans
Mammary Glands, Human / cytology*,  metabolism,  physiology
Mechanotransduction, Cellular / genetics,  physiology*
Oligonucleotide Array Sequence Analysis
Phenotype
Risk Factors
Grant Support
ID/Acronym/Agency:
CA076537/CA/NCI NIH HHS; R01 CA076537-07/CA/NCI NIH HHS; R01 EB000184-01/EB/NIBIB NIH HHS; T32 CA009681-11/CA/NCI NIH HHS; T32CA009681/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
EC 2.7.1.112/PTK2 protein, human; EC 2.7.10.1/Focal Adhesion Kinase 1; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases
Comments/Corrections

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


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