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. 2016 Feb 7;7(9):10472–10485. doi: 10.18632/oncotarget.7228

Figure 3. Effect of the Shh pathway on c-Met and AKT phosphorylation.

Figure 3

KAT-18 A. and SW1736 B. cells were treated with 0.5% DMSO, cyclopamine (5 μM) or GANT61 (10 μM) for 72 hr. The cells were harvested and analyzed for AKT (S473) phosphorylation, c-Met tyrosine phosphorylation at Y1230/1234/1235m and Gli1 expression by Western blot with their specific antibodies. The density of the bands from three independent experiments was analyzed and plotted in a bar graph. *p < 0.05; **p < 0.01. C. KAT-18 cells stably transfected with encoding a control, Shh or Gli1 miRNA or transfected with pcDNA3.1 or pcDNA/Gli1 were analyzed for AKT and c-Met phosphorylation by Western blot with their specific antibodies. Actin was included as a loading control.

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