Tumor progression in vivo: increased soybean agglutinin lectin binding, N-acetylgalactosamine-specific lectin expression, and liver metastasis potential.

摘要: Abstract Tumors which grew out from threshold s.c. inocula of L5178Y-F9 and SL2–5 murine T-cell lymphomas in syngeneic DBA/2 mice exhibited a unified natural defense-resistant phenotype including an increased tumorigenicity correlating reductions susceptibility to antibodies, killer cells, activated macrophages vitro . The metastatic potential cell surface saccharide expression these cells were determined assess the impact growth small tumor focus vivo on subsequent ability determine whether there was any association with changes carbohydrates, have been implicated now for many years development. A significantly liver-colonizing observed following i.v. injection. most consistent change detected studies using five lectins increase N -acetyl-d-galactosamine (d-GalNAc)-specific soybean agglutinin (SBA) binding. log experimental liver metastasis, SBA binding, percentage hepatocyte rosetting parental -selected significant direct correlations. While inhibition lines by d-GalNAc galactose involvement d-galactose/d-GalNAc-specific receptor, preincubation but not hepatocytes inhibited homotypic These data suggest role saccharide-specific, lectin-like receptor both interactions therefore metastasis. Furthermore, d-GalNAc-inhibitable binding sites variants should d-GalNAc-specific receptors providing rationale relationship between potential.