Figure 4

Statins specifically suppress the activation of Ras/extracellular signal-regulated kinase (ERK) and Ras/Akt pathways in C6 glioma cells. (A) C6 glioma cells were treated with 5 μM mevastatin, 5 μM fluvastatin, or 10 μM simvastatin for 1, 3, 6, 12, or 24 h. Control cells were treated with 0.1% DMSO and cultured in serum-containing medium for 24 h. Whole-cell lysates were generated and immunoblotted with antibodies against phosphorylated ERK1/2 (phospho-ERK1/2), phosphorylated Akt (phospho-Akt), phosphorylated c-Jun N-terminal kinase 1/2 (phospho-JNK1/2), ERK1/2, Akt, and JNK1/2. (B) ERK1/2 and Akt activation in C6 cells to which statins were administered with or without the addition of MVA, FPP, and GGPP. Phospho-ERK1/2, phospho-Akt, ERK1/2, and Akt levels were determined by immunoblotting analysis of the whole-cell lysate.