Involvement of gicerin, a cell adhesion molecule, in the portal metastasis of rat colorectal adenocarcinoma cells.

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.