Expression and function of α2,3‐sialyl‐ and α,3/l,4‐fucosyltransferases in colon adenocarcinoma cell lines: Role in synthesis of E‐selectin counter‐receptors

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Abstract
We show here that colon‐carcinoma cell lines adhere to E‐selectin via sialyl Lewis x and sialyl Lewis a (sLex and sLea) oligosaccharides and that this adhesion can be enhanced by TNF stimulation. To study in greater detail this endothelial binding, we analysed the mRNA expression and function of the enzymes participating in the generation of sLex and sLea on cancer cells. These oligosaccharides are synthesized by sequential action of α2,3 sialyl (α2,3‐ST) and α1,3/1,4 fucosyltransferases (α1,3/1,4‐FT) on existing (poly)N‐acetyllactosamine chains. We report here that mRNAs of 2 recently cloned α2,3‐STs and 4 α1,3/l,4‐FTs are expressed in adenocarcinoma cells. In functional assays α2,3‐ST and α1,3‐ or 1,4‐FT activities were observed in adenocarcinoma cell lysates to exogenous N‐acetyllactosamine and lacto‐N‐biose acceptors and to their sialytated derivatives, leading to the synthesis of the sialyl‐N‐acetyllactosamine and sLex or the sialyllacto‐N‐biose and sLea, respectively. Furthermore, the inflammatory cytokine TNF could enhance some α2,3‐ST and α1,3/1,4‐FT activities capable of generating E‐selectin counter‐receptors. Taken together, these data show that COLO 205 and HT‐29 adenocarcinoma cell lines adhere to E‐selectin in a TNF‐inducible manner via their cell‐surface sLex and sLea. These cells also express mRNA as well as inducible enzyme activities of several α2,3‐STs and α,3/1,4‐FTs responsible for the final steps in the synthesis of sLex and sLea. We show here that the TNF‐induced adhesion to E‐selectin might be due to the increased synthesis of sLex and sLea in colon‐carcinoma cells.

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