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Tenascin: growth and adhesion modulation--extracellular matrix degrading function: an in vitro study
P Shrestha1, S Sumitomo, C H Lee
1Department of Oral and Maxillofacial Surgery, Asahi University School of Dentistry, Tsukuba City, Japan.
European Journal of Cancer. Part B, Oral Oncology
|March 1, 1996
Summary
Tenascin (TN), an extracellular matrix protein, promotes tumor cell growth and detachment. Its enhanced expression in cancer may influence tumor progression, adhesion, invasion, and metastasis.
Area of Science:
- Cell Biology
- Biochemistry
- Cancer Research
Background:
- Tenascin (TN) is an extracellular matrix protein with restricted adult expression, but upregulated in neoplastic lesions.
- The precise functions and molecular mechanisms of enhanced TN expression in cancer remain unclear.
Purpose of the Study:
- To investigate the biological roles of Tenascin (TN) in vitro using various cell lines.
- To elucidate the effects of TN on cell growth, adhesion, and extracellular matrix degradation in neoplastic cells.
Main Methods:
- In vitro studies using human carcinoma (SCCKN), adenocarcinoma (SGT-1), and mouse fibroblast cell lines (NIH3T3-3, Cle-H3).
- Assessing TN secretion in response to transforming growth factor-beta.
- Analyzing cell adhesion on substrates coated with fibronectin (FN), laminin (LN), and TN.
- Investigating the induction of collagenase secretion by tumor cells on FN/TN substrates.
Main Results:
- Transforming growth factor-beta dose-dependently enhanced TN secretion in all cell lines.
- TN exhibited growth-enhancing activity and inhibited cell-to-cell contact.
- Cells adhered poorly to TN, with high TN concentrations inhibiting adhesion to FN in cancer cells.
- Neoplastic cells on FN/TN substrates secreted collagenase, unlike non-neoplastic cells.
Conclusions:
- Enhanced Tenascin (TN) expression in neoplastic lesions may promote tumor growth and detachment.
- TN can interfere with fibronectin's role in cell adhesion, potentially impacting cell morphology.
- The induction of collagenase by TN in cancer cells suggests a role in extracellular matrix degradation and tumor invasion.