Loss of strain specificity of the TA3-St subline: evidence for the role of epiglycanin in mouse allogeneic tumor growth

Abstract

We described the in vivo conversion of the strain-specific ascites murine mammary adenocarcinoma subline TA3-St to a new ascites subline designated TA3-MM. This conversion occurred during passage in a syngeneic A/HeHa mouse infected with pneumonia-producing microorganisms. The mode number of chromosomes of the TA3-MM cell (82) was greater than that of the parental TA3-St cell (69) or the other non-strain-specific subline TA3-Ha (42). The TA3-MM subline could grow in and kill mice of various allogeneic strains. In addition, the TA3-MM cell possessed numerous receptors for the lectin of Vicia graminea seeds, which were hardly detectable at the surface of the parent TA3-St subline but were present in abundance at the cell surface of the non-strain-specific subline TA3-Ha. These lectin receptors of the TA3-Ha cell were previously demonstrated to be present in a unique high-molecular-weight endogenous cell surface glycoprotein termed epiglycanin. The V. gramines lectin receptors on the new TA3-MM subline also were present on an epiglycanin-like molecule. This finding provides further evidence for the hypothesis that allogeneic growth in the TA3 system is a direct result of these membrane glycoproteins.