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Alterations in the Expression of a Hepatocyte Cell Adhesion Molecule by Transplantable Rat Hepatocellular Carcinomas¹

University of Texas System Cancer Center, Science Park, Research Division, Smithville, Texas 78957 [D. C. H., K. D. M.], and Department of Medical and Physiological Chemistry, University of Uppsala, The Biomedical Center, Uppsala, Sweden [B. Ö.]

Alterations in the expression of normal cell surface components on 13 transplantable hepatocellular carcinomas were examined using a heteroantiserum [anti-M_r 105,000 glycoprotein (gp105)] reactive with a family of nine wheat germ agglutinin binding components from normal rat hepatocytes with an average molecular weight of 105,000. Analysis by two-dimensional polyacrylamide gel electrophoresis of components immunoprecipitated by anti-gp105 antiserum from detergent extracts of transplantable hepatocellular carcinoma cells surface labeled with ¹²⁵I revealed qualitative and quantitative changes in the expression of anti-gp105-reactive components with the most consistent change being the apparent loss of a pair of acidic (pl 4.1 to 4.3) glycoproteins by all 13 transplantable hepatocellular carcinoma lines. One-dimensional peptide maps of fragments produced following digestion with V8 protease indicated that these acidic components were closely related in structure but differed significantly from other anti-gp105-reactive components. Immunodepletion analysis with monoclonal antibodies and heteroantisera reactive with individual components recognized by anti-gp105 antiserum showed that the two acidic glycoproteins were antigenically and structurally identical to cell-CAM 105, a M_r 105,000 glycoprotein involved in cell-cell adhesion of rat hepatocytes. Antibodies raised against purified cell-CAM 105 were specific in immunoprecipitation assays for the acidic components, strongly inhibited reaggregation of hepatocytes, and displayed no reactivity by indirect immunofluorescence or immunoprecipitation analysis with transplantable hepatocellular carcinoma cells. These results suggest that major alterations in the expression of cell-CAM 105 may be a consistent feature of the malignant phenotype.

¹ This research was supported by Grant CA 31103 from the NIH, the Swedish Medical Research Council (Project 05200, 6686), and Konung Gustaf Vis 80-arsfond.

² To whom requests for reprints should be addressed.

Received 12/10/84. Revised 3/26/85. Accepted 4/ 3/85.

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