Modulation of intracellular second messengers by dietary fat during colonic tumor development.
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In conclusion, dietary n-3 polyunsaturated fatty acids found in fish oil are capable of suppressing carcinogen-induced ras activation in the colon prior to overt neoplasia. This in turn blocks the oncogene driven increase in colonic diacylglycerol mass, preventing the persistent activation and chronic down-regulation of PKC isozymes, thereby maintaining tissue PKC levels. Since the maintenance of crypt PKC levels may sustain the homeostatic balance between cell proliferation, differentiation and apoptosis, the ability of dietary n-3 polyunsaturated fatty acids to block the carcinogen-induced decrease in steady-state levels of colonic mucosal PKC may in part explain why these fatty acids protect against colon tumorigenesis. Additional studies are required in order to elucidate the mechanisms by which select dietary lipids reduce colonic tumor incidence. This research focus is absolutely essential, because if we do not know why a dietary component is protective or promotive of cancer, then we have no right to attempt to modify eating behaviors.