Health & Environmental Research Online (HERO)


Print Feedback Export to File
1649102 
Journal Article 
Colitis-associated colon tumorigenesis is suppressed in transgenic mice rich in endogenous n-3 fatty acids 
Nowak, J; Weylandt, KH; Habbel, P; Wang, J; Dignass, A; Glickman, JN; Kang, JX 
2007 
Yes 
Carcinogenesis
ISSN: 0143-3334
EISSN: 1460-2180 
28 
9 
1991-1995 
English 
17634405 
WOS:000250676300020 
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-kappaB), 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-kappaB activity. These results support a protective role of n-3 PUFA supplementation in the prevention of CRC.