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Journal of Histochemistry and Cytochemistry, Vol. 47, 1575-1580, December 1999, Copyright © 1999, The Histochemical Society, Inc.

ARTICLE

Expression of the Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) and the Matrix Metalloproteinase-2 in Bronchopulmonary and Breast Lesions

Stéphanie Caudroya, Myriam Polettea, Jean-Marie Tourniera, Henriette Burleta, Bryan Tooleb, Stanley Zuckerc, and Philippe Birembauta
a INSERM U 514, IFR 53, Laboratoire Pol Bouin, CHU de REIMS. Reims, France
b Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts
c Departments of Research and Medicine, Veterans Affairs Medical Center, Northport, New York

Correspondence to: Myriam Polette, INSERM U 514, IFR 53, Laboratorie Pol Bovin, CHU de Reims, 45 rue Cognacq-Jay, 51100 Reims, France.

Tumor cells interact with stromal cells via soluble or cell-bound factors stimulating the production of matrix metalloproteinases (MMPs), a group of enzymes largely involved in the extracellular matrix (ECM) remodeling in tumor invasion. Among these factors, extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to stimulate in vitro the fibroblast production of various MMPs such as interstitial collagenase (MMP-1), stromelysin-1 (MMP-3), and gelatinase A (MMP-2). In this study, the EMMPRIN protein was detected by immunohistochemistry prominently in malignant proliferations of the breast and the lung. It was present at the surface of both tumor epithelial and peritumor stromal cells. Because previous studies have reported that stromal cells do not express EMMPRIN mRNAs, it is very likely that EMMPRIN is bound to stromal cells via a specific receptor. Moreover, our observations also demonstrated that the same peritumor stromal cells strongly express MMP-2. Our results show that EMMPRIN is an important factor in tumor progression by causing tumor-associated stromal cells to increase their MMP-2 production, thus facilitating tumor invasion and neoangiogenesis. (J Histochem Cytochem 47: 1575–1580, 1999)

Key Words: metalloproteinases, tumor invasion, breast cancer, lung cancer


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