Fig. 6

Compound-1H inhibited AKT and ERK signaling pathways in human glioblastoma cells. U87 and LN229 cells were treated with different concentrations (0, 15, 30 and 60 μmol/L) of the compound-1H for 48 h. The expression levels of Ras, c-Raf, P-Raf, Akt, P-Akt, ERK, and P-ERK were determined by western blot. β-Tubulin was used as a loading control. The results were representative of three independent experiments