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[Cancer Research 56, 2556-2560, June 1, 1996]
© 1996 American Association for Cancer Research
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Cyclooxygenase-2 Overexpression and Tumor Formation Are Blocked by Sulindac in a Murine Model of Familial Adenomatous Polyposis1

Susan K. Boolbol, Andrew J. Dannenberg, Amy Chadburn, Charles Martucci, XiaoJun Guo, John T. Ramonetti, Maria Abreu-Goris, Harold L. Newmark, Martin L. Lipkin, Jerome J. DeCosse and Monica M. Bertagnolli2

Strang Cancer Prevention Center [S. K. B., A. J. D., C. M., J. T. R., H. L. N., M. L. L., M. M. B.] and The New York Hospital-Cornell University Medical Center [S. K. B., A. J. D., A. C., X. G., J. T. R., M. A-G., M. L. L., J. J. D., M. M. B.], New York, New York 10021

Inducible cyclooxygenase (Cox-2), also known as prostaglandin H synthase 2 (PGH-2) is a key enzyme in the formation of prostaglandins and thromboxanes. Cox-2 is the product of an immediate-early gene that is expressed in response to growth factors, tumor promoters, or cytokines. Overexpression of Cox-2 is associated with both human colon cancers and suppression of apoptosis in cultured epithelial cells, an activity that is reversed by the nonsteroidal anti-inflammatory drug, sulindac sulfide. To address the relationship between Cox-2, apoptosis, and tumor development in vivo, we studied C57BL/6J-Min/+(Min) mice, a strain containing a fully penetrant dominant mutation in the Apc gene, leading to the development of gastrointestinal adenomas by 110 days of age. Min mice were fed AIN-76A chow diet and given sulindac (0.5 ± 0.1 mg/day) in drinking water. Control Min mice and homozygous C57BL/6J-+/+ normal littermates lacking the Apc mutation (+/+) were fed AIN-76A diet and given tap water to drink. At 110 days of age, all mice were sacrificed, and their intestinal tracts were examined. Control Min mice had 11.9 ± 7.8 tumors per mouse compared to 0.1 ± 0.1 tumors for sulindactreated Min mice. As expected, +/+ littermates had no macroscopic tumors.

Examination of histologically normal-appearing small bowel from Min animals revealed increased amounts of Cox-2 and prostaglandin E2 compared to +/+ littermates. Using two different in situ techniques, terminal transferase-mediated dUTP nick end labeling and a direct immunoperoxidase method, Min animals also demonstrated a 27–47% decrease in enterocyte apoptosis compared to +/+ animals. Treatment with sulindac not only inhibited tumor formation but decreased small bowel Cox-2 and prostaglandin E2 to baseline and restored normal levels of apoptosis. These data suggest that overexpression of Cox-2 is associated with tumorigenesis in the gastrointestinal epithelium, and that both are inhibited by sulindac administration.

1 Supported by American Cancer Society Clinical Career Development Award ACS CDA-95010-95 (to M. M. B.).

2 To whom requests for reprints should be addressed, at The New York Hospital-Cornell Medical Center, 525 East 68th Street, Suite F-1913, New York, NY 10021.

Received 1/22/96. Accepted 4/ 3/96.




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