Fucose and galactose receptor and liver recognition by lymphoma cells

A syngeneic model system for the study of metastases is described. The system consisted of 2 lymphoma clones (A/63-I and A/63-2) derived from a single thymoma (A/63) induced by a wild-type Abelson-Moloney viral complex. Phenotype and genotype analyses revealed that both clones were derived from transformation of early T-cell precursors. An in vivo study of the colonizing potential following intravenous (i.v.) injection of clones showed that only the A/63-I cell clone colonized the liver. This observation was confirmed by quantitative analysis of organ distribution of both cell clones consecutive to i.v. injection of 125IUdR-labelled cells. In the same way, an in vitro study of the invasive potential of both clones was performed on frozen liver sections and showed that only the A/63-I cell clone had the ability to attach to liver. This specific adhesion was inhibited by L-fucose, D-galactose, N-acetyl-D-galactosamine (D-GalNAc) and with D-galactose- and L-fucose-containing neoglycoproteins. Differences in cell surface carbohydrates of the 2 cell clones were detected using various lectins: peanut agglutinin (PNA), Dolichos biflorus (DBA), Aleuria aurantia (AAA) and Galactia tenuiflora agglutinins (GTA). A/63-I was found to react strongly with PNA, DBA and GTA, and the removal of sialic acid by neuraminidase treatment increased DBA and PNA receptor sites of A/63-2 as compared to A/63-I. The present data suggest that cell-surface GalNAc, galactosyl and fucosyl residues are responsible for the ability of the A/63-I cell clone to recognize liver tissue probably through binding to a Kupffer-cell-associated lectin.