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. 2013 Oct 12;6:78. doi: 10.1186/1756-8722-6-78

Figure 7.

Figure 7

CK2 inhibition hampers STAT3 activation upon daunorubicin treatment of AML cells. (A) Representative immunoblot analysis of phospho Ser727 STAT3 (pSTAT3 Ser727), total STAT3, MCL1, SOCS3 protein levels in ML-2 cells untreated, exposed to increasing concentrations of daunorubicin (0.05-0.1-0.15 μM) in the absence or presence of CX-4945 5 μM (top panels) or K27 4 μM (bottom panels). (B) Real time quantitative PCR analysis of MCL1 (lefmost panels) and SOCS3 (rightmost panels) mRNA in ML-2 cells untreated, exposed to increasing concentrations of daunorubicin (0.05 and 0.15 μM) in the absence or presence of CX-4945 5 μM (top panels) or K27 4 μM (bottom panels). (C) Immunoblot analysis of phospho Ser727 STAT3 (pSTAT3 Ser727), total STAT3 and MCL1 in freshly isolated AML blasts from a patient left untreated or exposed to increasing concentrations of daunorubicin (0.05-0.1 μM) in the absence or presence of CX-4945 5 μM. In all the experiments data represent mean ± SD, n = 3. * indicates p < 0.05.