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Studies on Protein Kinase C and Colon Carcinogenesis
Jose G. Guillem, MD;
Catherine A. O'Brian, PhD;
Cheryl J. Fitzer;
Mark D. Johnson, PhD;
Kenneth A. Forde, MD;
Paul LoGerfo, MD;
I. Bernard Weinstein, MD
Arch Surg. 1987;122(12):1475-1478.
Abstract
• To further understand the molecular mechanisms of bile acid—mediated colon tumor promotion, we have examined the possible role of protein kinase C (PKC) in this process. Protein kinase C has been implicated in tumor promotion because it is the receptor for the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate (TPA) and mediates the action of this compound as well as that of other tumor promoters and growth factors. Our studies show that, in a manner analogous to 12-0-tetradecanoyl-phorbol-13-acetate, deoxycholic acid (DOA) can induce a time-dependent cellular redistribution of PKC as well as a concentration-dependent overexpression of the ornithine decarboxylase gene. These results taken together with our previous findings demonstrating decreased levels of PKC in human colon carcinomas compared with adjacent normal mucosa provide evidence that PKC has a role in colon carcinogenesis.
(Arch Surg 1987;122:1475-1478)
Author Affiliations
From the Department of Surgery, Columbia-Presbyterian Medical Center (Drs Guillem, Forde, and LoGerfo), and the Institute of Cancer Research, Columbia University (Drs Guillem, O'Brian, Johnson, and Weinstein and Ms Fitzer), New York.
Footnotes
Accepted for publication Aug 12, 1987.
Read before the Annual Meeting of the Society of Surgical Oncology, London, April 29, 1987.
Reprint requests to Department of Surgery, Columbia-Presbyterian Medical Center, Columbia University, 622 W 168th St, New York, NY 10032 (Dr Guillem).
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