FIGURE 6.

Relationship between phosphorylation of intracellular signal kinases and lysophosphatidylcholine (lysoPC) effects through long‐chain acyl‐coenzyme A synthases 5 (ACSL5). Levels of phosphorylated (p‐) phosphoinositide 3‐kinase (PI3K), Akt, mTOR, GSK‐3β, TSC2, Raf, MEK, ERK, RSK and MSK proteins were measured in SPC‐A1 cells 6 h after treatment with lysoPC. Regulatory effects of PI3K and ERK in reactive oxygen species (ROS) production quantified by DCF fluorescence intensity (B), ACSL5 gene expression (C) and cell proliferation rate (D) were assayed in SPC‐A1 cells pretreated with PI3K inhibitor LY294002 or ERK inhibitor GDC0994 for 2 h and followed by lysoPC treatment for 6 h (n = 6) or in ACSL5 ^NC or ACSL5 ^KD cells pretreated with inhibitors of PI3K and ERK for 2 h (n = 6). Protein levels of ACC and FASN in SPC‐A1 cells pretreated with vehicle or PI3K/ERK inhibitors were measured 6 h after lysoPC treatment (E). * and ** or # and ## stand for the p‐values less than .05 and .01, respectively, as compared with cells treated with vehicle or lysoPC