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Carcinoembryonic Antigen–Related Cell Adhesion Molecule 1^a-4L Suppression of Rat Hepatocellular Carcinomas

Division of Hematology and Oncology, Department of Medicine, Rhode Island Hospital/Brown University Medical School, Providence, Rhode Island

Requests for reprints: Douglas C. Hixson, Department of Medicine, Rhode Island Hospital/Brown University Medical School, 593 Eddy Street, Providence, RI 02903. Phone: 401-444-8058; Fax: 401-444-8141; E-mail: dhixson{at}lifespan.org.

Carcinoembryonic antigen (CEA)–related cell adhesion molecule 1 (CEACAM1) is a member of the CEA family of immunoglobulin-like adhesion molecules with two major splice variants, CEACAM1^a-4L and CEACAM1^b-4S, differing in the length of their COOH-terminal cytoplasmic tail. Both forms are down-regulated in prostate and liver carcinomas relative to normal tissues. We have previously shown in a nude mouse xenograft model that restoration of CEACAM1^a-4L expression in human prostate carcinoma cells (PC-3) suppresses tumorigenicity, an effect observed with carcinomas from several other tissues but never established for hepatocellular carcinomas. In this report, we have examined the effect of CEACAM1^a-4L on tumorigenicity of 1682A, a rat hepatocellular carcinoma that grows on the omentum when injected into the peritoneal cavity. Results show that restoration of CEACAM1^a-4L expression at levels 13- and 0.45-fold compared with negative controls or normal hepatocytes, respectively, completely suppressed the formation of 1682A tumor nodules on the omentum at 3 weeks after injection. In contrast, 1682A cells infected with CEACAM1^b-4S or an empty retroviral vector formed multiple clusters of tumor nodules. Although tumor nodules of 1682A cells positive and negative for CEACAM1^a-4L did not display significant differences in histologic organization, aggregates formed in vitro by 1682A-L were smaller in size and displayed enlarged intercellular spaces relative to their 1682A-V counterparts. Restoration of CEACAM1^a-4L expression did not elevate levels of apoptosis but seemed to cause an increase in the length of G₁. This is the first demonstration of CEACAM1^a-4L–induced tumor suppression in liver carcinomas using a quantifiable i.p. syngeneic transplantation model.

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