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Tenascin‐C matrix assembly in oral squamous cell carcinoma
Author(s) -
Ramos Daniel M.,
Chen Bing,
Regezi Joseph,
Zardi Luciano,
Pytela Robert
Publication year - 1998
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(19980302)75:5<680::aid-ijc4>3.0.co;2-v
Subject(s) - tenascin c , fibronectin , tenascin , extracellular matrix , cell culture , biology , microbiology and biotechnology , pathology , laminin , matrix (chemical analysis) , integrin , cell , chemistry , medicine , biochemistry , genetics , chromatography
We previously showed that the extracellular matrix component tenascin‐C (TN‐C) is upregulated in oral squamous cell carcinoma (SCC) compared with the normal oral mucosa. In this study we examined oral biopsy specimens of mild to moderate dysplasia or carcinoma in situ to study TN‐C expression. We found that carcinoma in situ is the stage at which TN‐C becomes widely expressed, suggesting it may be involved in the initial stages of tumor progression. To study TN‐C matrix production in vitro, we used an invasive oral SCC cell line (HSC‐3) and peri‐tumor fibroblasts (PTF). Neither cell type organized a TN‐C matrix when cultured alone; however, when co‐cultured with HSC‐3 cells, PTF were able to assemble a TN‐C matrix. PTF retained the ability to organize a TN‐C matrix when separated from the HSC‐3 cells by a semi‐permeable membrane, indicating that cell‐cell contact is not necessary for TN‐C matrix organization and suggesting that soluble factors may be involved. Moreover, PTF were induced to assemble TN‐C matrices when grown in medium conditioned by both the PTF and HSC‐3 cells. Antibodies to fibronectin (FN) and to the first FN type III repeat blocked both FN and TN‐C matrix assembly, indicating that TN‐C matrix organization is dependent on an FN template. Antibodies to α5, αv and β1 integrins also blocked TN‐C matrix formation. When seeded onto FN matrices, the co‐cultures were unaffected by the anti‐integrin and anti‐FN antibodies and were able to organize a TN‐C matrix. Our results suggest that progression of malignant oral SCC is accompanied by an alteration of the normal ECM to one rich in TN‐C, and that the organization of a TN‐C matrix is dependent on soluble cues provided by both the SCC cells and the PTF. Int. J. Cancer 75:680–687, 1998.© 1998 Wiley‐Liss, Inc.