Fucosylated histo-
blood group antigens such as Lewis b, Lewis Y, and H accumulate in colon
carcinoma and this is accompanied by a clear increase in alpha(1-2)fucosyltransferase activity, a key
enzyme for the biosynthesis of these
antigens. Yet the
biological significance of alpha(1-2) fucosylated structures is not well defined. We have transfected a poorly tumorigenic rat colon
carcinoma cell line with the human
H blood group alpha(1-2)fucosyltransferase
cDNA. This resulted in cell surface expression of H
antigens with a concomitant decrease of
sialic acid substituted and free beta-
galactosides. Immunoprecipitation experiments showed that H
antigens were essentially borne by variants of CD44 carrying amino acid sequences encoded by exon v6. The transfected cells showed increased motility in a wound healing assay, without changing their proliferation rates. Parental and control cells transfected with an empty vector formed small
tumors that always regressed after 30 days when injected subcutaneously to syngeneic rats. In contrast, alpha(1-2)fucosyltransferase transfectants were able to form progressive
tumors. Increased tumorigenicity was also visible in nude mice. These results demonstrate that alpha(1-2)fucosylated
antigens contribute directly to aggressiveness of colon
carcinoma cells. This could occur by altering a function of CD44 variants.