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. 2016 Feb 3;7(9):10073–10089. doi: 10.18632/oncotarget.7164

Figure 5. Silencing one pathway confers Abl transformants more sensitive to inhibition of the other pathway.

Figure 5

A. K562 cells stably expressing luciferase-specific shRNA or PDK1-specific shRNAs were treated with 15 μM SMI-4a for indicated time and immunoblotted for eIF4B phosphorylation. B. K562 cells in A were treated by indicated concentrations of SMI-4a for 48 h. Cells were harvested and apoptosis was displayed as percent viability using Annexin V staining followed by FACS. Values represent means ± SEM, n = 3 (*P < 0.05, **P < 0.01). C–F. K562 cells (C) or W44 cells (E) ectopically expressing shRNA targeting luciferase or Akt1 were treated with 15 μM SMI-4a (K562) or 8 μM SMI-4a (W44) in a time course, and analyzed by Western blotting as described in A. Cells were treated with indicated concentrations of SMI-4a for 48 h (K562) or 24 h (W44), and apoptosis of K562 (D) or W44 (F) was evaluated by FACS. G. and H. S6K1 knockdown or control K562 cells were incubated with 15 μM SMI-4a for indicated time and analyzed as described in A and B. I–L. K562 cells stably expressing luciferase-specific shRNA or Pim-1-specific shRNAs were treated with 10 μM Akti-1/2 (I) or 10 μM rapamyicn (K) for indicated time, and immunoblotted for eIF4B phosphorylation. Cells were incubated with Akti-1/2 for 48h (J) or rapamyicn for 36h (L) at indicated concentrations. Cell apoptosis was examined as described in B.