Gicerin, an Ig-superfamily
cell adhesion molecule, has homophilic adhesion activity, thus leading to the formation of
gicerin aggregates.
Gicerin is highly expressed in various embryonic tissues, and it contributes to development through its adhesive activities. In contrast, the expression of the
protein is limited to the muscular tissues and endothelial cells in the mature animals. In the liver,
gicerin is constitutively expressed in sinusoidal endothelial cells. Interestingly, an overexpression of
gicerin is found in a variety of
tumors and may play a role in
tumorigenesis. Previously, up-regulated expression of the
gicerin protein was found in some sporadic cases of chicken colorectal
adenocarcinomas and their hepatic metastasized lesions. In the present study,
gicerin cDNA was introduced into endogenous
gicerin negative ACL-15 cells, a rat
colon adenocarcinoma cell line. The cells were subsequently evaluated for changes in their metastatic potentials in order to elucidate the possible role of
gicerin in the hepatic
metastasis of colorectal
adenocarcinomas. The stable overexpression of
gicerin in the cells enhanced the self-aggregation and migratory activities on the
protein compared with the mock-transfectants. In addition, the
gicerin- transfectants had enhanced metastatic potential to the liver compared with mock-transfected cells after implantation into the ileocolic vein of the cognate rats. These results suggest that
gicerin might promote the interaction of
tumor cells with a hepatic endothelium, thus leading to the hepatic
metastasis of
colon adenocarcinomas.