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. 2020 Feb 13;14(4):779–794. doi: 10.1002/1878-0261.12640

Figure 2.

Figure 2

CCL5 mediates partial protection from PKC412 induced growth suppression and apoptosis in FLT3‐ITD‐positive MOLM‐13 cells (A) PKC412‐sensitive MOLM‐13 cells were cultured in the presence of 50 ng/mL CCL5 ± 500 nm TAK‐779 and simultaneously treated with PKC412 at the indicated concentrations. MOLM‐13 cells cultured without CCL5 and treated with PKC412 served as a control. After 48 h, proliferation was measured in MTS analysis. Three independent experiments were performed in triplicates. (B) TKI‐sensitive MOLM‐13 cells were cultured in the presence of CCL5 at 50 ng/mL for 14 days followed by treatment with PKC412 at the indicated concentrations. Proliferation was measured using MTS assay 48 h after addition of PKC412. (C) Sensitive MOLM‐13 cells were cultured in the presence of CCL5 at 50 ng/mL for 14 days or left untreated and after 14 days were exposed to PKC412 (50, 100 nm) for 36 h. Flow cytometric analysis of vital (Annexin‐PE‐negative, 7‐AAD‐negative) and apoptotic cells (Annexin‐PE‐positive, 7‐AAD‐positive) was performed. (D) Same experiments as in C, depicted as bar chart. Annexin‐PE+/7‐AAD+ cells labeled as total apoptotic cells, single Annexin‐PE+ cells labeled as early apoptotic cells, single 7‐AAD+ cells labeled as late apoptotic cells. Significant differences are marked with (*): *P < 0.05, **P < 0.01, ***P < 0.001. Student’s t‐test. Error bars represent SD. N = 3 for (A,B and D).