Fig. 2: Combinations of CDK8/19i and BCR-ABLi cooperatively induce apoptosis and inhibit phosphorylated STAT1 and STAT3 S727 in K562 cells. | Cell Death Discovery

Fig. 2: Combinations of CDK8/19i and BCR-ABLi cooperatively induce apoptosis and inhibit phosphorylated STAT1 and STAT3 S727 in K562 cells.

From: CDK8/19 inhibition attenuates G1 arrest induced by BCR-ABL antagonists and accelerates death of chronic myelogenous leukemia cells

Fig. 2

K562 cells were treated with CDK8/19i and/or BCR-ABLi for 24 h. A Cell cycle distribution/PI staining followed by flow cytometry. Shown are the percentages of subG1 events in untreated cells (control) and cells treated with 1 µM IM, 1 nM dasatinib (das), 50 nM nilotinib (nilo) or 10 nM PF-114 alone or with 1 µM SenB. Note an increased subG1 fraction in combinations of all BCR-ABLi and SenB. B Immunoblotting showed that IM, das, nilo and PF-114, each in combination with SenB, inhibited STAT1 S727 phosphorylation and induced the cleavage of PARP1, caspases 9 and -3. SenB and SNX631 (S631) in combination with IM elevated C subG1 proportion and D apoptotic markers. E SenB together with IM (I + S) decrease the amounts of pSTAT1 S727, STAT1 and pSTAT3 S727. GAPDH and β-actin are loading controls. Statistical analysis was performed using one-way ANOVA. **p < 0.01, ***p < 0.001, ****p < 0.0001. Values are mean ± SD, n = 3.

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