OVEREXPRESSION OF SYNDECAN-2 SUPPRESSES THE METASTATIC PHENOTYPE OF MOUSE LEWIS LUNG CARCINOMA CELLS

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The syndecan family of cell surface heparan sulfate proteoglycans participates in adhesion-dependent and growth factor-stimulating events by acting as physiological receptors for extracellular matrix molecules and growth factors. Bifunctional glycosyltransferases, the D-glucuronyl- and N-acetyl-D-glucosaminyl transferases, essential for chain elongation of heparan sulfate have been recently demonstrated to be encoded in the EXT family of tumor suppressors. Alterations in the formation of the heparan sulfate glycosaminoglycan due to mutation of EXT genes have been thus implicated in tumor formation. Therefore, it is possible that both quantitative and qualitative alterations of the glycosaminoglycan are involved in tumor progression. Indeed, we demonstrated in this study that mouse Lewis lung carcinoma 3LL-derived different metastatic clones showed an inverse correlation between the metastatic potentials and the expression level of syndecan-2. The causal relation for this correlation was established by demonstration that overexpression of syndecan-2 by transfection of its cDNA into the highly metastatic LM66-H11 cloned cells caused striking suppressions of both experimental and spontaneous metastases. In addition, the overexpressers became to resemble the low metastatic P29 cells in several in vitro phenotypes such as the fibronectin-mediated actin cytoskeletal organization, doubling time, saturation density, and cell morphology. The results indicate that syndecan-2 is directly involved in regulation of those phenotypic expressions, and sugget that the degree of metastasis is determined by the tumor architecture directed by these in vitro phenotypes.
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OVEREXPRESSION OF SYNDECAN-2 SUPPRESSES THE METASTATIC PHENOTYPE OF MOUSE LEWIS LUNG CARCINOMA CELLS

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