Analysis for expression of apoptosis and cytokines in target mucosal epithelium of large bowel carcinogenesis

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Expression of cytokines was examined in methylazoxymethanol (MAM) acetate and/or 1-hydroxyanthraquinone (1-HA)-induced large bowel neoplasms and carcinogen exposed non-neoplastic epithelium of the bowel in rats. Both cytokines of TNF-a and IL-la was more expressed in the carcinogen-initiated non-neoplastic epithelium than in the normal epithelium. The expression of the cytokines in the neoplasms was stronger than in the non-neoplastic epithelium. The results suggest a mutual relationship between the expression of the cytokines and carcinogenesis.Arachidonic acid is induced by activation of phospholipase C (PLC) as well as phospholipase A_2. We discovered that expression of PLC-delta, one of 3 isozymes of PLC of the neoplasms is lower than of the non-neoplastic tissues in the large bowel carcinogenesis of rats. These results also imply that expression of imflammation associated enzymes and cytokines is related to cell growth or carcinogenesis in the large bowel.Relationship between the cell proliferation and the apoptosis was investigated in mucosal epithelium of large bowel on the initial stage of azoxymethane-induced carcinogenesis. Apoptosis was induced 4 hours after the exposure of carcinogen and reached to the peak at after 8 hours. In 3 days, appearance of apoptosis was decreased and increased the cell proliferation reversely. AOM-induced apoptosis appeared to relate to inhibition of mitosis. PCNA was found to be not the biomarker for cell proliferation in the early stage of AOM-induced toxicity which is associated with cell-cycle arrest.