ABSTRACT
Investigations of dietary fat consumption and cancer risk and progression point to a critical role for both the quantity and the quality of dietary fat in modulating cancer. In particular, omega-6 (ω-6) polyunsaturated fatty acids (PUFAs) are highly suspect to be the underlying culprits for dietary promotion of cancer. Conversely, evidence suggests that omega-3 (ω-3) PUFAs oppose the effects of ω-6 PUFAs. Clinical studies, although with some mixed results, have largely supported these claims. Animal studies investigating the effects of dietary PUFAs have consistently demonstrated the cancer-promoting and -protective effects of ω-6 and ω-3 PUFA, respectively, in a variety of cancer types. Although the mechanisms underlying these apparent cancer-modulating phenotypes by PUFAs remain to be further claried, several hypotheses have been postulated, including regulation of membrane signaling, oxidative stress, production of proinammatory and anti-inammatory signaling molecules, and immune regulation. In this chapter, we will review PUFA metabolism to various downstream metabolites and their potential roles in modulating cancer risk and progression.
Fatty acids are lipid molecules typically consisting of a single carbon chain with a carboxylic acid functional group at the alpha carbon. Saturated fatty acids (SAFAs) contain completely hydrogenated carbons with no double bonds, whereas monounsaturated fatty acids (MUFAs) and PUFAs contain one or more than one double bond, respectively. There are two main types of PUFAs: ω-3 and ω-6. Each group is characterized by the placement of the rst double bond in the carbon chain
