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. 2016 Apr 9;7(20):29102–29115. doi: 10.18632/oncotarget.8667

Figure 5. The activation of p38MAPK and JNK contribute to carfilzomib and vorinostat-induced apoptosis.

Figure 5

(A) Pretreatment with U0126, SB203580, and SP600125 (10 μM each) for 2 h, after which MOLT-4 cells were treated with 6 nM carfilzomib or/and 0.4 μM vorinostat for 48 h, then cell apoptosis was monitored by Annexin V/PI staining. (B) MOLT-4 cells stably expressing p38MAPK shRNA or scrambled sequence were treated with 6 nM carfilzomib or/and 0.4 μM vorinostat for 48 h, then cell apoptosis was monitored by Annexin V/PI staining. Inset: Relative expression of p38MAPK protein in MOLT-4 cells stably expressing p38MAPK shRNA and scrambled sequence. (C) After treatment as in B, the expression of p-p38MAPK and PARP proteins was monitored by western blot. (D) MOLT-4 cells stably expressing JNK shRNA or scrambled sequence were treated as in B, then cell apoptosis was monitored by Annexin V/PI staining. Inset: Relative expression of JNK protein in MOLT-4 cells stably expressing JNK shRNA and scrambled sequence. (E) MOLT-4 cells stably expressing JNK shRNA or scrambled sequence were treated as in B, and then the expression of JNK and PARP proteins was monitored by western blot. * represent p < 0.05; ** represent p < 0.01; *** represent p < 0.001; # represent p > 0.05.