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Heterogeneity in the Induction and Expression of Carcinoembryonic Antigen-related Antigens in Human Colon Cancer Cell Lines¹

Gastrointestinal Research Laboratory (151M2), Veterans Administration Medical Center, San Francisco, California 94121, and the Department of Medicine, University of California, San Francisco, San Francisco, California 94143 [N. W. T., T. L. S., J. R. G., S. B. H., Y. S. K.]; Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, California 91010 [J. E. S.]; and Division of Hematology/Oncology, University Hospitals of Cleveland, Cleveland, Ohio 44106 [J. K. V. W.]

Sodium butyrate induces morphological and biochemical changes consistent with a more differentiated phenotype in some colon cancer cell lines. These changes include increased expression of carcinoembryonic antigen (CEA) and other oncodevelopmental markers. We utilized domain-specific probes and polyclonal antibodies against CEA-related antigens to study sodium butyrate-induced expression of the CEA gene family in a villous adenoma-derived cell line, which is nontumorigenic in nude mice (VACO 235), and two colonic carcinoma cell lines known to respond to sodium butyrate exposure by phenotypic differentiation (HT-29 and LS 174T). The induction begins as quickly as 24 h after exposure and occurs primarily at a transcriptional level, although some translational control is also evident. No evidence was found for gene amplification, rearrangement, or methylation to account for the mechanism of this transcriptional control. [³⁵S]Cysteine pulse-labeled cell lysate immunoblots and polyadenylated RNA blot hybridization suggest that increases in mRNA transcript and CEA-related glycoprotein levels are primarily due to increased synthesis rather than decreased degradation. A considerable amount of heterogeneity is seen in the biosynthesis of the CEA-related glycoproteins, with each cell line showing a distinct pattern of CEA-related antigen expression from a limited number of mRNA transcripts.

¹ This work was supported by the Veterans Administration Medical Research Service; NIH Institutional Training Grant 5 T32 DK07007; American Cancer Society Grant PDT-293; and National Cancer Institute Grants CA45967, CA47551, and CA37808. N. W. T. is an Associate Investigator of the Veterans Administraiton, and Y. S. K. is a Medical Investigator of the Veterans Administration.

² To whom requests for reprints should be addressed, at G. I. Research Laboratory (151M2), Veterans Administration Medical Center, 4150 Clement St., San Francisco, CA 94121.

Received 9/ 2/88. Revised 3/ 1/89. Accepted 3/22/89.

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