We have previously reported that
colon cancer cells metastasized to the liver expressed an increased amount of
sialyl Lewis X (SLeX)
antigen compared to their corresponding primary lesions. It is now well known that SLeX
antigen and
sialyl Lewis A (SLeA)
antigen are
ligands for the
selectins expressed on the endothelial cells. Therefore, it is assumed that SLeX-rich
colon cancer cells could be easily adhered to the endothelial cells that express
selectins. In this report we have tried to induce
selectin expression on the human liver sinusoidal endothelial cells and have examined the adhesion of SLeX-high or -low expressing
colon cancer cells to the
interleukin-1beta (IL-1beta)-treated liver specimens using Stamper-Woodruff assay. These human
colon cancer cells are termed KM12HX or KM12LX cells, respectively. A significantly increased number of KM12HX cells adhered to the IL-1beta-treated liver specimens compared to KM12LX cells. The adhesion of KM12HX cells was inhibited by the pretreatment of
tumor cells with anti-SLeX antibody or by the pretreatment of liver specimens with anti-
selectin antibodies.
Selectin expression on the liver sinusoidal endothelial cells and endothelial cells of blood vessels after IL-1beta treatment was confirmed by immunohistochemically using anti-
selectin monoclonal antibodies (MAbs). These findings strongly suggest that SLeX-expressing
cancer cells could adhere to the sinusoidal endothelial cells via an SLeX-
selectin interaction system and this could be a first step for
colon cancer cells that metastasize to the liver. The mechanism by which these
selectins can be induced in vivo is the next problem to be considered.