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Fucose and galactose receptor and liver recognition by lymphoma cells
Author(s) -
Vavasseur F.,
Berrada A.,
Heuze F.,
Jotereau F.,
Meflah K.
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910450429
Subject(s) - clone (java method) , sialic acid , fucose , asialoglycoprotein receptor , galactosamine , microbiology and biotechnology , galactose , cell , biology , biochemistry , chemistry , in vitro , dna , hepatocyte
A syngeneic model system for the study of metastases is described. The system consisted of 2 lymphoma clones (A/63‐1 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/63‐1 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 125 IUdR‐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/63‐1 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/63‐1 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/63‐1. The present data suggest that cell‐surface GalNAc, galactosyl and fucosyl residues are responsible for the ability of the A/63‐1 cell clone to recognize liver tissue probably through binding to a Kupffer‐cell‐associated lectin.