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Adenoma-specific Alterations of Protein Kinase C Isozyme Expression in Apc^MIN Mice¹

Brown University, Providence, Rhode Island 02912 [I. K. K.]; Mayo Clinic, Scottsdale, Arizona 85259 [S. R. R., S. J. G.]; and Laboratory Medicine and Pathology [L. J. B., S. C. Z., P. C. R.] and Department of Medicine, Division of Gastroenterology [W. E. K.], Mayo Clinic, Rochester, Minnesota 55905

Members of the protein kinase C (PKC) family appear to play important roles in colorectal carcinogenesis. To investigate the potential involvement of PKC isozymes in adenomatous transformation induced by inactivation of the adenomatous polyposis coli (APC) gene product, we examined protein levels and localizations of ten PKC isozymes by immunohistochemistry in normal and adenomatous ileal epithelium of Apc^MIN mice. Compared with surrounding normal epithelium, adenomas showed dramatically reduced staining for PKCs , ß1, and , as well as dysplasia-specific punctate nuclear staining of PKC µ. We conclude that reduced protein expression of PKC , ß1, and , and nuclear localization of PKC µ are markers of, and are perhaps involved in, adenomatous transformation induced by APC inactivation in Apc^MIN mice.

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