Cell signal mechanisms, conjugated linoleic acids (CLAs) and anti-tumorigenesis.
Fats have been adversely implicated in the aetiology of many forms of cancer yet evidence is accumulating that certain types of fatty acids have anticancer properties. This is well documented for fish-oil fatty acids of the n-3 family. Recently, fatty acids found to occur naturally in ruminant-derived food products were found to have anticancer properties. These fatty acids were identified as conjugated linoleic acids (CLAs) derived from the parent linoleic acid by its partial hydrogenation by rumen bacteria. Studies with tumour-bearing animals have shown that consumption of CLAs particularly with regard to breast and prostate cancer is beneficial. Studies with cancer cells have also shown that these fatty acids can inhibit cell proliferation and induce cell death. However, little is known regarding the mechanisms of action of these CLAs. In particular, which cellular signal mechanisms are regulated by CLAs which can explain their anticancer properties. We have shown that CLAs specifically up-regulate cell signal systems at the level of gene expression (mRNA, protein) in human breast and prostate cancer cells which are responsible for the induction of apoptosis or programmed cell death. These findings support the anticancer effects of CLA found in animal models and indicate similar effects could occur in man.
D000818:Animals; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D004041:Dietary Fats / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D008041:Linoleic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D009369:Neoplasms / Q000178:diet therapy* / Q000209:etiology / Q000517:prevention & control; D015398:Signal Transduction / Q000187:drug effects*
D000970:Antineoplastic Agents; D004041:Dietary Fats; D008041:Linoleic Acids