Fig. 4.

The anti-proliferative effect of AMPK activation is mediated by inhibition of lipogenesis. (A) Schema showing how AICAR can potentially regulate lipogenesis. (B) Thin layer chromatography of total cellular lipids from serum starved cells showed increased intracellular fatty acids in EGFRvIII expressing cells, which was inhibited by AICAR treatment for 24 h. (C) Addition of mevalonate and palmitate rescued AICAR-mediated growth inhibition. U87-EGFRvIII and U87-EGFR cells were plated, 24 h later they were treated with AICAR (0.5 mM) alone or in combination with mevalonate and/or palmitate (100 μM). Cells were treated for 3 days and relative cell growth was determined by the WST assay (Chemicon). *, P < 0.001 compared with control; # P < 0.01. (D) Inhibition of HMG-CoA reductase (atorvastatin 1 μM) and acetyl-CoA carboxylase (ACC) (TOFA 10 μg/mL) preferentially blocked the growth of EGFR-activated glioblastoma cells. Control cells were treated with DMSO (1:1,000).