Oleic acid inhibits store-operated calcium entry in human colorectal adenocarcinoma cells.

Much evidence indicates the association between dietary fat and colorectal cancer risk. However, most of the studies focus on polyunsaturated fatty acids, and little is known about the role of monounsaturated ones and their precise mechanism of action. Being store-operated Ca²⁺ entry (SOCE) a Ca²⁺ influx pathway involved in the control of multiple cellular and physiological processes including cell proliferation, we studied the effect of oleic acid in Ca²⁺ signals of colorectal cancer cells, paying particular attention to SOCE. Carbachol was used to induce SOCE in Fura 2-loaded HT29 cells. We tested a saturated fatty acid to compare the physiological relevance of our results. We show that oleic acid is a potent inhibitor of SOCE. By contrast, stearic acid failed to have a SOCE-inhibitory effect. The SOCE-inhibition induced by oleic acid was protein kinase C-independent and restored by albumin. We also demonstrated that oleic acid induced increases in [Ca²⁺](i). The novelty of our report is that little variability in the concentration could end in a large different physiological effect. In conclusion, we suggest a physiological pathway for the beneficial effect of oleic acid in colon carcinoma cells.