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Tumor Biology |
Department of Molecular Genetics, Nagoya City University Medical School, Nagoya 467-8601 [K-i. K., T. M., T. K., T. O.], and Department of Surgery, 2nd Teaching Hospital, Fujita Health University Medical School, Nagoya 454-8509 [K-i. K., T. M., S. M.], Japan
Although the beneficial effect of cimetidine on survival in cancer has
been clinically demonstrated in colorectal cancer patients, the mode of
action of cimetidine has not been elucidated. In this report, we have
demonstrated for the first time that cimetidine can block the adhesion
of a colorectal tumor cell line to the endothelial cell monolayer in
cell culture and that it can suppress the metastasis of the tumor cell
in a nude mouse model. We also demonstrated that these antimetastasis
effects of cimetidine might occur through down-regulation of the cell
surface expression of E-selectin on endothelial cells, a ligand for
sialyl Lewis antigens on tumor cells. We found that the
cimetidine-mediated down-regulation of E-selectin did not involve
down-regulation of E-selectin mRNA or blocking of the nuclear
translocation of nuclear factor 
B, a transcriptional activator of
E-selectin gene expression. Because two other histamine type 2 receptor
antagonists, famotidine and ranitidine, did not show any similar
effect, these actions of cimetidine probably do not occur via
blocking of the histamine receptor. These observations support the idea
that cancer metastasis can be blocked by cimetidine administration
through blocking the adhesion of tumor cells to the endothelium when an
interaction between E-selectin and sialyl-Lewis antigens plays a role.
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