Administration of SF1126 and LY294002 blocked the activation of AKT and inhibited the in vitro growth of glioma cells from12 V-Ha-Ras transgenic mice. A. Left panel shows that treatment of SF1126 and LY294002 (25 μM and 50 μM) significantly decreased the levels of phospho-AKT. Right panel shows the densitometry analysis of pAKT band relative to AKT. Bottom panel shows endogenous levels of phospho-AKT and PTEN in the derivative glioma cells from the 12 V-Ha-Ras transgenic mice as compared to the primary astrocytes from the wild type animal. B. Left panel shows the effect of pre-pulse of RGDS peptide on the inhibition of levels of phospho-AKT following the treatment of SF1126 and LY294002 in glioma cells from the 12 V-Ha-Ras transgenic mice. Cells were pulsed with RGDS peptide (50 μM) for 30 minutes prior to the treatment of SF1126 (25 μM) or LY294002 (25 μM). Phospho-AKT levels were determined 30 minutes after the treatment of the inhibitors. Right panel shows the densitometry analysis of pAKT band relative to AKT. C. Effects of SF1126 and LY294002 on the in vitro growth of the derivative glioma cells from the 12 V-Ha-Ras transgenic mice. Derivative glioma cells were treated (50 μM) with SF1126 or LY294002 and the growth of the cells were determined from the cell counts (trypan blue) 24, 48 and 72 hours following the administration of the inhibitors. Bars represent the mean ± SD of readings from 4 independent experiments. *P < 0.05. Experiments were repeated three times with similar results.