Abstract
Mucopolysaccharides (i.e., glycosaminoglycans) have recently been implicated with various aspects of tumor cell-host interactions. First, the presence of tumor cell-associated mucopolysaccharides may be related to the regulation of cellular growth and invasiveness of tumors. Particular mucopolysaccharides seem to play specific roles at the tumor cell periphery. For example, the mucopolysaccharide heparan sulfate (HS) has been shown to be structurally heterogeneous mainly due to the differences in 6-O-sulfation and N-sulfation of glucosamine, and the variations in HS sulfation have been found to be tissue specific and related to the malignant potentials of tumor cells. Qualitative and quantitative changes in HS may affect the microenvironment of cells and modify cellular interactions, growth and differentiation. Secondly, glycosaminoglycans such as HS constitute a major fraction of the endothelial cell basement membrane which acts as a barrier against the invasion of blood-borne tumor cells. We have found that metastatic tumor cells with high lung colonization potentials possess specific abilities to degrade both HS proteoglycans in the basal lamina-like matrix of cultured endothelial cells and purified, soluble lung HS. This observation may explain how metastatic tumor cells migrate through the vascular wall and develop metastatic lesions in distant, often specific, organ sites. In this review we discuss the roles of tumor cell-associated mucopolysaccharides and mucopolysaccharide degrading enzymes in tumor cell-host interactions which lead to metastasis.
