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. 2017 Jan 14;8(9):14604–14619. doi: 10.18632/oncotarget.14654

Figure 5. The D4476-dependent reduction of β-catenin and AKT is independent from the proteasome and is mediated by caspase and p53.

Figure 5

(A) Expression of phospho β-catenin on Ser45 (p β-catenin S45), phospho β-catenin on Ser33/37/Thr41 (p β-catenin S33/37/T41), phosphorylated AKT on Ser473 (p AKT S473) and total β-catenin and AKT in H929 (left panel) and INA-6 cells, grown alone (middle panel) or in co-culture with HS-5 (INA-6/HS-5, right panel), treated with D4476 for 48 h and BZ for 18 h or the combination of the two compounds at the concentrations indicated in the Figure. (B) Expression of total β-catenin, AKT, Pro-caspase 3 and Mcl1 proteins in INA-6 cells treated with D4476 20 μM in association with Z-VAD-FMK for 48 h. In the combination treatment, cells were pretreated with Z-VAD-FMK 2 μM for 1 h before the addition of D4476. (C) INA-6 and H929 cells were treated with doxorubicin (Doxo) 1.2 μM for 18 h. β-catenin, p53, Mdm2, and p21 were evaluated by WB. In all experiments GAPDH was used as loading control.