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Departments of Medicine [R. N. D., J. S., J. D. M.], Surgery [H. S., J. S., R. D. B.] and Cell Biology [R. D. B., R. N. D.], and Molecular Toxicology Center [R. N. D.], Vanderbilt University Medical Center and Veterans Affairs Medical Center, Nashville, Tennessee 37232-2279
Previously, we have shown that forced expression of prostaglandin endoperoxide synthase-2 [also called cyclooxygenase (COX) 2] leads to inhibition of programmed cell death in intestinal epithelial cells. More recently, we have demonstrated that growth of human colonic cancer xenografts is inhibited by treatment with a highly selective COX-2 inhibitor in tumors that express COX-2 (HCA-7) but not in those that lack COX-2 expression (HCT-116). To explore the biochemical mechanisms involved in these effects, we have evaluated the role of COX-2-derived eicosanoid products on programmed cell death in human colon cancer cells. Here we report that PGE2 treatment of human colon cancer cells leads to increased clonogenicity of HCA-7, but not HCT-116 cells. Treatment with a highly selective COX-2 inhibitor (SC-58125) decreases colony formation in monolayer culture and this growth inhibition was reversed by treatment with PGE2. Additionally, PGE2 inhibits programmed cell death caused by SC-58125 and induces Bcl-2 expression, but did not affect Bcl-x or Bax expression in human colon cancer (HCA-7) cells. Therefore, decreased cell death caused by PGE2 would enhance the tumorigenic potential of intestinal epithelial cells. Thus, these results may help to explain a component of the mechanism by which COX inhibitors prevent colorectal cancer in humans.
1 This study was supported by USPHS Grants DK-47297 (to R. N. D.), GM-53319 (to R. D. B.), CA-69457 (to R. D. B.), DK-48831 (to J. D. M.), GM-15431, and GM-42056 (to J. D. M.); National Institute of Environmental Health Sciences Grant 00267; and the Veterans Affairs Merit Grant (to R. N. D.).
2 To whom requests for reprints should be addressed, at the Department of Medicine/GI, MCN C-2104, Vanderbilt University Medical Center, Nashville, TN 37232-2279. Phone: (615) 343-8989; Fax: (615) 343-6229; E-mail: duboism@ctrvax.vanderbilt.edu.
Received 7/22/97. Accepted 11/11/97.
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