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[Cancer Research 52, 5971-5978, November 1, 1992]
© 1992 American Association for Cancer Research

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Mucin Gene Expression in Colonic Tissues and Cell Lines1

S. Ogata, H. Uehara, A. Chen and S. H. Itzkowitz2

Gastrointestinal Research Laboratory, Department of Medicine [S. O., A. C., S. H. I.], and Department of Molecular Biology [H. U.], Mount Sinai School of Medicine, New York, New York 10029

Complementary DNA clones encoding four different mucin core peptides have been isolated. However, the expression of these mucin genes in the colon has not been systematically studied. The present investigation used Northern blot analysis to study the expression of MUC1, MUC2, MUC3, and MUC4 mRNA in paired normal and cancerous colonic tissues, and nine colon cancer cell lines. Results were correlated with the clinicopathological features of the tumors and with the immunohistochemical expression of several carbohydrate tumor-associated antigens that may reside on mucins. MUC1 mRNA was expressed in all colonic tissues, and levels in paired normal and cancer tissues were similar in most cases. MUC2 and MUC3 mRNAs were expressed in both normal and cancer tissues, but levels were often decreased in the cancers. MUC4 mRNA was present in normal mucosa with comparable or sometimes greater expression in cancers. There was no apparent correlation between the expression of any particular mucin gene or pattern of mucin genes and the site, stage, or histological type of tumor. In addition, the expression of mucin-associated carbohydrate antigens did not correlate with any individual mucin gene or group of mucin genes. In colon cancer cell lines all four MUC genes were expressed rather weakly or not at all. These results indicate that the human colon expresses a broad repertoire of mucin genes which are differentially regulated in malignancy. Whether this differential regulation of mucin genes affects the behavior of the tumor and results in the altered glycosylation commonly seen in these tumors requires further investigation.

1 Supported in part by National Cancer Institute Grant CA54291, the Aaron Diamond Foundation, and the Chemotherapy Foundation. S. H. I. is a recipient of an Irma T. Hirschl Career Scientist Award.

2 To whom requests for reprints should be addressed, at GI Research Laboratory, Box 1069, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029.

Received 4/13/92. Accepted 8/26/92.




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Copyright © 1992 by the American Association for Cancer Research.