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. 2016 Mar 15;7(14):17290–17300. doi: 10.18632/oncotarget.8039

Figure 4. Activation of STAT3, AKT or MEK1 protects cells from [ruxolitinib + MMF], maintains SOD2, TRX, BCL-XL and MCL-1 expression and prevents expression/activation of BIM and BAD.

Figure 4

A. SUM149 and BT474 cells were transfected with an empty vector plasmid (CMV) or with plasmids to express: activated STAT3; activated AKT; or activated MEK1. Twenty four h after transfection cells were treated with vehicle control or with ruxolitinib (1.0 μM) and MMF (5.0 μM) in combination for 24h. Twenty four h later cell viability was assessed using a live/dead assay in a Hermes WiScan microscope at 10X magnification (n = 3 +/− SEM). B. SUM149 cells were transfected with an empty vector plasmid (CMV) or with plasmids to express: activated STAT3; activated AKT; or activated MEK1. Twenty four h after transfection cells were treated with vehicle control or with ruxolitinib (1.0 μM) and MMF (5.0 μM) in combination for 12h. Cells were fixed in place and permeabilized using 0.5% Triton X100. Immuno-fluorescence was performed to detect the expression of SOD2, TRX, BCL-XL and MCL-1 at 10X magnification in the Hermes WiScan machine (n = 3 +/− SEM). C. SUM149 cells were transfected with an empty vector plasmid or with plasmids together to express activated AKT and to express activated MEK1. Twenty four h after transfection cells were treated with vehicle control or with ruxolitinib (1.0 μM) and MMF (5.0 μM) in combination for 12h. Cells were fixed in place and permeabilized using 0.5% Triton X100. Immuno-fluorescence was performed to detect the expression of BIM and the S112 S136 phosphorylation of BAD (n = 3 +/− SEM).