This review focuses on the recent advances in investigations of the role of cell surface
carbohydrates in
tumor metastasis. It also summarizes the results of extensive studies of endogenous
lectins, their structure,
carbohydrate specificity and
biological functions with the major emphasis on the significance of
lectin-cell surface
carbohydrate interactions in a metastatic process. Numerous data demonstrate that malignant transformation is associated with various and complex alterations in the glycosylation process. Some of these changes might provide a selective advantage for
tumor cells during their progression to more invasive and metastatic phenotype. Cell glycosylation depends on the expression and function of various
glycosyltransferases and
glycosidases. Recently, transfection of genes encoding various glysosyltransferases gene in sense and antisense orientation helped to bring direct evidence that changes in cell surface
carbohydrates are important for the metastatic behavior of
tumor cells. Cell surface
carbohydrates affect
tumor cell interactions with normal cells or with the extracellular matrix during metastatic spread and growth. These interactions can be mediated via
tumor cell
carbohydrates and their
binding proteins known as endogenous
lectins. The family of the discovered endogenous
lectins is rapidly expanding. The number of
C-type lectins has reached 50 and at least 10
galectins have been identified. The
biological significance of the endogenous
lectins and their possible role in
tumor growth and
metastasis formation has started to unravel. Some
lectins recognize the 'foreign' patterns of cell surface
carbohydrates expressed by microorganisms and
tumor cells, and play a role in innate and adaptive immunity. It was shown that
lectins affect
tumor cell survival, adhesion to the endothelium or extracellular matrix, as well as
tumor vascularization and other processes that are crucial for metastatic spread and growth.