Data published in a recent issue of Cancer Research reported that researchers at Texas A&M University, using GE Healthcare's CodeLink microarrays, have identified key changes in gene expression that provide an improved understanding of how dietary fat composition affects the initiation and promotional stages of tumor development in the colon. These findings indicate that the chemopreventive effect of fish oil is due to the direct action of a particular type of polyunsaturated fatty acid, n-3 PUFA.
Second only to lung cancer, colon cancer is a major cause of cancer death in the United States. According to the American Cancer Society, currently more than 106,370 people are diagnosed with colon cancer, and 56,730 die each year. Environmental factors, including diet, are known to influence colon cancer incidence, and the discovery of how diet influences the progression of the disease may ultimately bring researchers closer to understanding methods of promoting prevention and halting progression.
"This study provides the medical community with insight into the underlying mechanisms that regulate the onset and progression of colon cancer," said Robert S. Chapkin, professor of Nutrition, Center for Environmental and Rural Health, Texas A&M University. "Until now, the challenge has been finding a method to identify and track the gene-related effect of dietary fat in the colonic epithelium. (The) microarrays provided us the advantage of detecting how dietary fat alters gene expression at the initiation and promotional stages of colon cancer. As a result, we were able to gather evidence that the chemopreventive effect of fish oil is due to the direct action of the fatty acid, n-3 PUFA, and not to a reduction in the content of n-6 PUFA."
In this preclinical study, researchers assigned animals (Sprague Dawley rats) to three dietary treatments differing only in the type of fat (corn oil/n-6 PUFA, fish oil/n-3 PUFA, or olive oil/n-9 monounsaturated fatty acid), two treatments (injection with the carcinogen azoxymethane or with saline), and two time points (12 hours and 10 weeks after first injection). Only the consumption of n-3 PUFA exerted a protective effect at the initiation and promotional stages. Importantly, analysis discerned fundamental differences among animals treated with n-3 PUFA at both the 12-hour and 10-week time points. Thus, in addition to demonstrating that dietary fat composition alters the molecular portrait of gene expression profiles in the colonic epithelium at both the initiation and promotional stages of tumor development, these findings indicate that the chemopreventive effect of fish oil is due to the direct action of n-3 PUFA and not to a reduction in the content of n-6 PUFA.