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. 2016 May 4;7(24):36185–36197. doi: 10.18632/oncotarget.9154

Figure 5. AIM2 inflammasome induced suppression of mTOR-S6K1 pathway.

Figure 5

(A–C) SMMC 7721 cells and HUH7 cells were transfected with EGFP-AIM2 plasmid or EGFP plasmid as mock control (A). 24 h after the transfection, activation of mTOR-S6K1-HIF1α pathway was detected by western blot, and band intensities of the key proteins were quantitatively analyzed with β-actin as an internal control and blank control group for standardization (B for SMMC7721 cells, C for HUH7 cells). (D–F) HepG2 cells and BEL7402 cells were transfected with AIM2 siRNA-2 or siRNA-3 to block the expression of AIM2, activation of mTOR-HIF1α pathway was detected by western blot (D), band intensities of the key proteins in mTOR-S6K1-HIF1α pathway were quantitatively analyzed with β-actin as an internal control and blank control group for standardization (E for BEL7402 cells, and F for HepG2 cells). (G–J) SMMC7721 cells and HUH7 cells were transfected with EGFP-AIM2 plasmid or empty plasmid before treatment with inflammasome inhibitors Yvad-CMK (50 μM) for 24 h. Western blot was used to detect the activation of mTOR-S6K1-HIF1α pathway (G for SMMC7721 cells and I for HUH7 cells). Band intensities of the key proteins were analyzed to show the differences among the indicated groups (H for SMMC7721 cells and J for HUH7 cells). ***P < 0.001 for statistical analysis of the indicated groups.