The modifying effect of dietary tuna (Thunnus thynnus orientalis) orbital oil rich in docosahexaenoic acid (DHA) and vitamin D3 (VD3) on the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) was investigated in male F344 rats. Animals were given three weekly subcutaneous injections of AOM (15 mg/kg body weight) to induce ACF. The rats were fed the experimental diet containing 5% tuna orbital oil (low fish oil), 23.5% tuna orbital oil (high fish oil), 5% corn oil (low corn oil) or 23.5% corn oil (high corn oil) for 5 weeks, starting 1 week before the first dose of AOM. Animals were sacrificed 2 weeks after the last AOM injection to count colonic ACF and assay the expression of cyclooxygenase (COX)-1 and -2. High corn oil diet significantly increased the development of ACF, when compared with low corn oil diet (P<0.005). High fish oil diet also increased ACF formation compared with low fish oil diet (P<0.01), but the increase was smaller than high corn oil diet. The frequency of ACF was significantly lower in the rats fed high fish oil diet than high corn oil diet (P<0.02). Moreover, frequency of ACF consisted of 4 or more crypts in rats fed the high fish oil diet was significantly lower than that of rats given high corn oil diet. COX-1 and COX-2 expression did not significantly differ among the groups. These results suggest that fish oil derived from tuna, which contains high amounts of DHA and VD3, suppresses the formation and growth of ACF without affecting COX-1 and COX-2 expression, and may have a preventive effect on colon carcinogenesis.

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CD44 participates in tumor cell adhesion to endothelial cells in the experimental metastatic process in B16BL6 melanoma cells.

There are several pieces of evidence suggesting a relationship between CD44 expression and tumor metastasis, but the role of CD44 in the metastatic processes is unclear. We analysed the role of CD44 in the experimental metastatic processes of B16BL6 melanoma cells using anti-CD44 monoclonal antibody (clone IM7). B16BL6 melanoma cells expressed CD44 and these cells treated with anti-CD44 monoclonal antibody increased in the experimental metastatic ability, indicating that CD44 participates in metastatic processes in B16BL6 cells. Furthermore, the adhesiveness of B16BL6 cells to endothelial cells and the retention of these cells in the lung increased by treatment with anti-CD44 monoclonal antibody. These results suggested that the CD44-mediated adhesion of tumor cells to endothelial cells was involved in the experimental metastatic process of B 16BL6 cells.

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