Studies of mammary carcinoma metastasis in a mouse model system. II: Lectin binding properties of cells in relation to the incidence and organ distribution of metastases.
A panel of fluorescein-conjugated lectins was used to investigate the cell surface carbohydrates of cell lines isolated from a mouse mammary adenocarcinoma which differ markedly in their morphological and metastatic properties. The lectin-binding profiles of the cells showed them to express generally similar cell surface characteristics; however, two minor differences were evident. Galactose moieties recognized by peanut lectin were expressed on all highly metastatic fusiform cell types examined, but only on 50-60 per cent of the polygonal cells of limited metastatic capacity. Similarly, N-acetylgalactosamine moieties were demonstrated on fusiform cell types by soya bean lectin binding but were not expressed on intact polygonal cells. In both cases pretreatment of polygonal cells with neuraminidase allowed lectin binding comparable with that of fusiform cells suggesting that Gal and GalNAc sugars were abundantly present but masked by sialic acid residues. Using a novel technique in which tumour cells were incubated on cryostat sections of normal tissues, it was found that the cell lines exhibited different adhesion patterns which to some extent reflected their preferential sites for spontaneous metastasis and organ colonization in vivo. Thus the adherence of fusiform cells to liver was five times as great as that of polygonal cells, whereas the latter bound preferentially to lung tissue. Prior treatment of polygonal cells with neuraminidase doubled their frequency of attachment to liver sections, but had no effect on their binding to other tissues. Also, the presence of 100 mM N-acetylgalactosamine during incubation specifically inhibited the adherence of fusiform cells to liver tissues, but did not significantly influence other cell-tissue interactions. The data suggest that the expression of galactosyl or N-acetylated galactosyl groups on the fusiform cells facilitates their attachment to lectin-like receptors on liver cells and contributes to their superior capacity, compared with polygonal cells, for growth and metastasis in this organ.
D000818:Animals; D050260:Carbohydrate Metabolism; D002462:Cell Membrane / Q000378:metabolism; D002999:Clone Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D006017:Glycolipids / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D037102:Lectins / Q000378:metabolism; D008113:Liver Neoplasms / Q000556:secondary; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D009362:Neoplasm Metastasis
D006017:Glycolipids; D006023:Glycoproteins; D037102:Lectins