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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Dawson, Dawn Willis, Joseph Dotson, Angela Newman, Robert A. Lovgren, Alysia Kern Lawrence, Earl Luo, Guangbin Myung, Seung-jae Yan, Min Guda, Kishore Pretlow, Theresa P. Platzer, Petra Dannenberg, Andrew J. Rerko, Ronald M. Markowitz, Sanford D. |
| Description | Author Affiliation: Myung SJ ( Department of Medicine, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH 44106, USA.); |
| Abstract | 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) is a prostaglandin-degrading enzyme that is highly expressed in normal colon mucosa but is ubiquitously lost in human colon cancers. Herein, we demonstrate that 15-PGDH is active in vivo as a highly potent suppressor of colon neoplasia development and acts in the colon as a required physiologic antagonist of the prostaglandin-synthesizing activity of the cyclooxygenase 2 (COX-2) oncogene. We first show that 15-PGDH gene knockout induces a marked 7.6-fold increase in colon tumors arising in the Min (multiple intestinal neoplasia) mouse model. Furthermore, 15-PGDH gene knockout abrogates the normal resistance of C57BL/6J mice to colon tumor induction by the carcinogen azoxymethane (AOM), conferring susceptibility to AOM-induced adenomas and carcinomas in situ. Susceptibility to AOM-induced tumorigenesis is mediated by a marked induction of dysplasia, proliferation, and cyclin D1 expression throughout microscopic aberrant crypt foci arising in 15-PGDH null colons and is concomitant with a doubling of prostaglandin E(2) in 15-PGDH null colonic mucosa. A parallel role for 15-PGDH loss in promoting the earliest steps of colon neoplasia in humans is supported by our finding of a universal loss of 15-PGDH expression in microscopic colon adenomas recovered from patients with familial adenomatous polyposis, including adenomas as small as a single crypt. These models thus delineate the in vivo significance of 15-PGDH-mediated negative regulation of the COX-2 pathway and moreover reveal the particular importance of 15-PGDH in opposing the neoplastic progression of colonic aberrant crypt foci. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 32 |
| Volume Number | 103 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2006-08-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Colonic Neoplasms Genetics Metabolism Hydroxyprostaglandin Dehydrogenases Physiology Animals Azoxymethane Carcinogens Colon Pathology Chemically Induced Cyclin D1 Ki-67 Antigen Biosynthesis Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Prostaglandins G Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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