A variety of studies have supported the finding that regular intake of aspirin or non-steroidal anti-inflammatory drugs can affect colorectal cancer carcinogenesis by decreasing the synthesis of prostaglandins (PGs). We report that PG F2alpha, in the presence of indomethacin, did not stimulate the proliferation in HCT-8 and HT-29 human colon adenocarcinoma cells. Moreover, in both cell lines fluprostenol, a specific agonist of FP receptors, did not increase intracellular Ca2+ concentration, monitored with the fluorescent dye fura-2. These results indicate that in HCT-8 and HT-29 cells: i) proliferation is not sensitive to PG F2alpha; ii) functional FP receptors are absent. Therefore, either PG F2alpha is not necessarily involved in the proliferation of colorectal mucosa or cell lines other than HCT-8 and HT-29 should be used to assess the role played by PG F2alpha in promoting cell proliferation in colon cancer.

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