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HNE and transferrin receptors on cells of colorectal carcinoma and CaCo2 cells treated with iron compound

Iron could act as mediator of oxidative stress and provoke cancer. However, iron compound - ferric-sorbitol-citrate (FSC) could inhibit proliferation of malignant cell. In many malignant tumors lot of transferrin receptors (TfR) has been identified in correlation with tumor differentiation. Looking for mechanism of antitumor effect of FSC, in this study we evaluated influence of FSC on TfR expression on CaCo2 and on primary colorectal carcinoma cells. We also examined the presence of HNE on CaCo2 cells treated or not with FSC as well as on colorectal carcinoma cells at different stages of disease. To examine the biological significance of HNE and TfR expression, immunohistochemical studies were performed. FSC decreased number of TfR on CaCo2 cells, but did not affect expression of TfR on non-malignant cells in vitro. Expression of TfR was dependent on FSC concentration and duration of the FSC presence. The same treatment of CaCo2 cells did not cause HNE generation. Strong cytoplasmic staining for TfR was revealed in all colorectal carcinomas, while in normal colon mucosa the reaction was positive only on the cell membrane. In samples of colorectal carcinoma HNE-protein adducts were found to be reduced if compared to the normal colon. These results suggest that iron serves as inducer of TfR expression. Reduced HNE production in tumor cells could protect them from cytotoxic effects of HNE, but antitumor effects of FSC do not seem to be mediated through lipid peroxidation.

iron; 4-hydroxynonenal; CaCo2

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