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. 2015 Apr 2;6(17):14953–14969. doi: 10.18632/oncotarget.3621

Figure 5. AKT and p38 MAPK contribute to the synergistic effects of GSI-I and BTZ in T-LPN.

Figure 5

A. Jurkat and HuT 78 cells treated with MK-2206 at 48 h showed a slight concentration-dependent decrease in their viability. The decrease in cell viability was more prominent after combined treatment with GSI-I and BTZ. However, in the presence of MK-2206, GSI and BTZ were able to further enhance their inhibitory effects on T-LPN cell viability. B. Western blot analysis showed a concentration-dependent decrease of pAKT after treating Jurkat and HuT 78 cells with MK-2206, and this decrease was more pronounced when a combination of GSI-I and BTZ were used. However, in the presence of MK-2206, GSI-I and BTZ completely abrogated the expression of pAKT. There were no changes in the basal levels of AKT proteins. GAPDH confirms equal protein loading. C. Jurkat and HuT 78 cells treated with SB203580 for 48 h demonstrated no significant changes in their viability. Although, combination treatment of GSI-I and BTZ drastically reduced cellular viability, this decrease was partially rescued in the presence of SB203580, GSI-I, and BTZ combined treatment. D. The expression of p-p38 MAPK demonstrated a concentration-dependent decrease after treatment with SB203580 alone. In contrast, the expression of p-p38 MAPK was remarkably increased after using GSI-I and BTZ to simultaneously treat the T-LPN cells. In the presence of SB203580, GSI-I, and BTZ collectively managed to partially rescue the expression of p-p38 MAPK. Changes were not observed in the basal levels of p38 MAPK protein. GAPDH was used as the loading controls. Data shown in (A) and (C) represent the means ± SE from three independent experiments (*: P < 0.001 vs. GSI-I + BTZ alone in both cells; †: P < 0.001 vs. MK-2206 [1 μM] or SB203580 [10 μM] in Jurkat; ‡: P < 0.0001 vs. MK-2206 [1 μM] or SB203580 [10 μM] in HuT 78).