BACKGROUND: Colorectal cancer is the second leading cause of cancer deaths in the United States. Anti-inflammatory drugs were shown to be effective in the prevention of colorectal cancer, supporting a link between inflammation and tumorigenesis in the colon. However, due to their side effects long-term administration of these drugs for colorectal cancer prevention is not feasible.

METHOD: 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, DSS) plus treatment with carcinogen (azoxymethane, AOM).

RESULTS: This was accompanied by lower activity of NF-B, higher expression of transforming growth factor beta (TGF-ß) in the colons, and lower expression of inducible nitric oxide synthase (iNOS) in the tumors of fat-1 animals.

CONCLUSION: Our data provide new insight into the mechanism by which n-3 PUFA suppress tumorigenesis through dampening of inflammation and NF-B activity. These results support a protective role of n-3 PUFA supplementation in the prevention of colorectal cancer.

PMID: 17634405

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