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. 2016 Nov 20;2016:5286972. doi: 10.1155/2016/5286972

Figure 2.

Figure 2

Effects of pathway inhibitors on phosphorylation of AKT, ERK1/2, and mTOR in human PPGL cells. (a–d) Dose-dependent inhibition of p-AKT (a), p-ERK1/2 (b), and p-mTOR (c, d) by pathway inhibitors (LY294002 (a), U0126 (b), AZD8055 (c), and sunitinib (d)). (e) Time course of phosphorylation of AKT, ERK1/2, and mTOR induced by the serum. (f) Effects of LY294002 (10 μM), U0126 (10 μM), AZD8055 (1 μM), and sunitinib (1 μM) on the phosphorylation of AKT, ERK1/2, and mTOR in human PPGL cells. β-Actin was used as a loading control. Because serum-stimulated cells had a conspicuous positive expression of p-AKT, p-ERK1/2, and p-mTOR, cells treated with the serum could naturally be taken as a positive control. The experiment was repeated three times. (g, h, i) The histograms represent the densitometric results of the phosphorylation from three independent experiments. ERK1/2, AKT, and mTOR phosphorylation in FBS group was taken as 100%. ∗ P < 0.05 versus FBS group; ∗∗ P < 0.01 versus FBS group.