In agreement with this, the overexpression of FUT1, which competes for the same substrate that α2,3-STs, in BxPC-3 pancreatic cancer cells resulted in a decrease in sLex levels, which was associated with a reduction in E-selectin-expressing CHO cells binding and an impaired metastatic potential into xenograft transplantation [51,52]. Here, SELE is linked to pancreatic neoplasm.