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Restricted expression of membrane type 1‐matrix metalloproteinase by myofibroblasts adjacent to human breast cancer cells
Author(s) -
Bisson Christèle,
Blacher Silvia,
Polette Myriam,
Blanc JeanFrédéric,
Kebers Florence,
Desreux Joëlle,
Tetu Bernard,
Rosenbaum Jean,
Foidart JeanMichel,
Birembaut Philippe,
Noel Agnès
Publication year - 2003
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11012
Subject(s) - myofibroblast , stromal cell , extracellular matrix , matrix metalloproteinase , pathology , immunohistochemistry , breast cancer , biology , cancer cell , breast carcinoma , cancer research , actin , in situ hybridization , cancer , chemistry , microbiology and biotechnology , medicine , gene expression , biochemistry , gene , genetics , fibrosis
The membrane type‐1 matrix metalloproteinase (MT1‐MMP), a protease originally identified in breast carcinoma, is characterized by its capacity to activate other MMPs (MMP‐2 and MMP‐13) and to degrade extracellular matrix. Our study was undertaken to localize and identify the MT1‐MMP expressing cells in human breast adenocarcinomas. A textural analysis of images obtained by immunohistochemistry and in situ hybridization showed precisely the co‐expression of alpha smooth muscle actin (αSM actin) and MT1‐MMP in myofibroblasts. MT1‐MMP expression is confined to myofibroblasts in close contact with tumor cells. In sharp contrast, the expression of MMP‐2 was more widely distributed in both αSM actin positive and negative cells close to and at distance from cancer cell clusters. Our in vitro observations are consistent with the higher level of MT1‐MMP expression and of MMP‐2 activation observed in αSM actin positive fibroblasts derived from breast tumors, as compared to normal breast fibroblasts. Collectively, these results implicate myofibroblasts as major producer of MT1‐MMP in breast cancer and emphasize the importance of stromal‐epithelial cell interactions in their progression. © 2003 Wiley‐Liss, Inc.