Journal Article

Colitis-associated colon tumorigenesis is suppressed in transgenic mice rich in endogenous <i>n</i>-3 fatty acids

Johannes Nowak, Karsten H. Weylandt, Piet Habbel, Jingdong Wang, Axel Dignass, Jonathan N. Glickman and Jing X. Kang

in Carcinogenesis

Volume 28, issue 9, pages 1991-1995
Published in print September 2007 | ISSN: 0143-3334
Published online July 2007 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgm166
Colitis-associated colon tumorigenesis is suppressed in transgenic mice rich in endogenous n-3 fatty acids

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Colorectal cancer (CRC) is the second leading cause of cancer deaths in USA. Anti-inflammatory drugs were shown to be effective in the prevention of CRC, supporting a link between inflammation and tumorigenesis in the colon. However, due to their side effects, long-term administration of these drugs for CRC prevention is not feasible. An increased tissue content of omega-3 polyunsaturated fatty acids (n-3 PUFA) can dampen colon inflammation in animals as well as in humans. Whether increasing colon tissue n-3 PUFA alone is effective in preventing colon tumorigenesis remains to be investigated. Here we show that endogenously increased tissue levels of n-3 PUFA in the fat-1 transgenic mouse model lower incidence and growth rate of colon tumors induced by inflammation (dextrane sodium sulfate) plus treatment with carcinogen (azoxymethane). This was accompanied by lower activity of nuclear factor kappa B (NF-κB), higher expression of transforming growth factor beta in the colons and lower expression of inducible nitric oxide synthase in the tumors of fat-1 animals. Our data provide new insight into the mechanism by which n-3 PUFA suppresses tumorigenesis through dampening of inflammation and NF-κB activity. These results support a protective role of n-3 PUFA supplementation in the prevention of CRC.

Journal Article.  3706 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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