B62

Consumption of 18C alpha linolenic, 20C eicosapentaenoic or 22C docosahexaenoic omega 3 fatty acids (n-3 FAs) has been shown to slow the growth of existing mammary tumors. It is likely that the reduction of cancer growth due to n-3 FAs uptake is not a consequence of one single significant mechanism since multiple mechanisms have been identified to suppress tumor growth. Preadipocytes or adipocytes make cytokines that promote the growth of tumor cells. For a better understanding the mechanisms of n-3 FAs suppression of tumorigeneses, this study was focused on the influence of canola oil (rich in n-3 FAs) versus corn oil (rich in n-6 FAs) on communication between preadipocytes/adipocytes and breast tumoral cell lines. The hypothesis was that canola oil and corn oil differentially affect the tumor microenvironment by modulating adipocyte secretion of inflammatory molecules.
 >Human white preadipocytes (HWP) were treated with serial doses of canola or corn oil (0, 25, 50, 100 μM) for 72 hours. The fat uptake was monitored by gas chromatography. It was a dose responsive increase in production of the proinflammatory cytokines, IL-6 and IL-11, in HWP treated with corn oil. There was no increase in IL-6 or IL-11 in HWP treated with canola oil. The production of IL-6 or IL-11 in fully differentiated adipocytes did not increase in response to either oil. T47D breast cancer cells (estrogen receptor positive) and MDA-MB-231 (estrogen receptor negative) were pretreated with the same concentration range of oil as the preadipocytes/adipocytes. The conditioned media from HWP and adipocytes was then used to treat two breast cancer cell lines for 72 hours. Analyses of these results are in progress. Decreasing of preadipocytes production of proinflammatory cytokines (IL-6, IL-11) by canola oil could represent a beneficial tool in cancer prevention. We expect that the results will provide the basis for an increased knowledge of n-3 FAs inhibition of tumorigeneses by a dietary change that humans could easily make. This research can open new avenues for breast cancer prevention via a better understanding at the cellular and molecular level of how the food influences cell communication. We are what we eat!

Sixth AACR International Conference on Frontiers in Cancer Prevention Research-- Dec 5-8, 2007; Philadelphia, PA