Figure 3.

Modulation of endogenous PUFA and its effect on TRPC3 mediated Ca²⁺ entry. (A) Western blot analyses demonstrate the presence of fatty acid hydoxylase (FAAH), cytoplasmic phospholipase A (cPLA) and COX2 in MCF-7 breast cancer cells. (B) COX2 protein levels were dramatically increased (almost 3-fold) 24 h after cells were transfected with COX2 plasmid. (C) Ca²⁺ entry evoked by store depletion was enhanced from control (pink line) by reduction of AA generation e.g. AACOCF3 (yellow line, 10 μM), COX2 expression (blue line). Nifedipine (purple line, 20 μM) did not affect Ca²⁺ entry but niflumic acid (blue line, 100 μM) as a COX2 inhibitor, slightly reduced the Ca²⁺ entry induced by store depletion. (D) All results were normalized to the controls. AACOCF3, PMSF (50 μM), and overexpression of COX2 significantly enhanced Ca²⁺ entry via activated TRPC induced by store depletion. Meanwhile niflumic acid reduced Ca²⁺ entry via TRPC induced by store depletion. Indomethacin and nifedipine did not affect Ca²⁺ entry via TRPC3.