Regulation of Colonocyte Apoptosis by Bcl-2: Influence of Chemotherapeutic Dietary Agents
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This study intends to elucidate a mechanism of cancer prevention by certain nutrients. The health benefits of n-3 polyunsaturated fatty acids, e.g., docosahexaenoic acid (DHA), and fiber are well documented. It has been previously documented that DHA and butyrate, a fiber by-product, work synergistically to prevent colorectal cancer by increasing cell death (apoptosis). The resulting increase in apoptosis could be caused in part by down-regulation of the anti-apoptotic protein bcl-2. This study aimed to determine the correlation of bcl-2 and the apoptotic effects of butyrate and DHA. Immortalized mouse colonocytes were pre-treated with DHA, transfected with human bcl-2 cDNA to overexpress full length bcl-2, and then co-treated butyrate. Apoptosis was measured using an enzyme-linked immunosorbent assay (ELISA), and western immunoblot was used to quantify bcl-2 levels. Apoptosis was significantly different (P<0.05) in DHA and butyrate treated cells depending on whether or not cultures were transfected with bcl-2. The DHA and butyrate treated cells transfected with bcl-2 contained significantly fewer apoptotic cells compared to untransfected DHA and butyrate treated cells. These data suggest that DHA and butyrate induce apoptosis in part by decreasing bcl-2 expression.
Turk, Harmony (2011). Regulation of Colonocyte Apoptosis by Bcl-2: Influence of Chemotherapeutic Dietary Agents. Available electronically from