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Expression of EMMPRIN by oral squamous cell carcinoma
Author(s) -
Bordador Leonardo C.,
Li Xiaowu,
Toole Bryan,
Chen Bing,
Regezi Joseph,
Zardi Luciano,
Hu Yongmei,
Ramos Daniel M.
Publication year - 2000
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/(sici)1097-0215(20000201)85:3<347::aid-ijc9>3.0.co;2-#
Subject(s) - matrix metalloproteinase , basigin , cell , chemistry , antibody , basement membrane , extracellular matrix , cell culture , epidermoid carcinoma , fibronectin , epithelium , microbiology and biotechnology , pathology , biology , carcinoma , immunology , medicine , biochemistry , genetics
A transmembrane glycoprotein recently identified on some tumor cells, extracellular matrix metalloproteinase inducer (EMMPRIN), has been shown to induce metalloproteinase (MMP) production by peritumor fibroblasts (PTF). We examined biopsy specimens of normal human oral mucosa and oral squamous cell carcinoma (SCC) for expression of EMMPRIN. In normal mucosa, EMMPRIN was expressed at the cell membrane throughout the epithelium with a slight enhancement along the basal cell layer. In oral SCC, EMMPRIN was expressed at the cell membrane throughout the entire lesion. Immunofluorescence microscopy localized EMMPRIN to the cell membrane in a highly invasive oral SCC cell line in agreement with our in vivo observations. Function‐blocking antibodies to EMMPRIN significantly inhibited oral SCC cell migration on tenascin‐C (TN‐C) and fibronectin as well as invasion through a reconstituted basement membrane (RBM). We previously showed that soluble factors from SCC cells and PTF are required for deposition of a TN‐C matrix. To determine whether EMMPRIN may modulate the release or expression of these soluble factors, we again used function‐blocking antibodies. Antibodies to EMMPRIN completely inhibited the organization of TN‐C matrices and partially reduced the deposition of FN matrices by oral SCC cell /PTF co‐cultures. In addition, antibodies to EMMPRIN perturbed the expression of MMP‐2. Moreover, antibodies to MMP‐2 perturbed oral SCC cell invasion of an RBM by approx. 75%. Our results demonstrate that EMMPRIN is highly expressed in oral SCC, facilitates tumor cell motility, and mediates TN‐C matrix deposition. Taken together, these results suggest that EMMPRIN may help regulate oral squamous cell carcinoma invasion. Int. J. Cancer 85:347–352, 2000. ©2000 Wiley‐Liss, Inc.