Fig. 5: SenB counteracts the effects of the exogenous CDKN1B (p27Kip1) on cell cycle and IM survival. | Cell Death Discovery

Fig. 5: SenB counteracts the effects of the exogenous CDKN1B (p27Kip1) on cell cycle and IM survival.

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

Fig. 5

A K562p27tet-on subline was treated with 1 µg/mL doxycycline (dox) and 1 µM IM for 24 h in the absence or presence of indicated concentrations of SenB followed by flow cytometry. SenB in a dose-dependent manner increases IM-induced apoptosis (subG1; right) and reduces G1 arrest (left). B K562p27tet-on cells were treated with IM, SenB (1 µM each) or their combination for 24 h in the absence or presence of vehicle (-dox) or 1 µg/mL doxycycline (+dox) followed by flow cytometry. Induction of p27Kip1 reduces IM-induced apoptosis (subG1 fraction). SenB partially alleviates the protective effect of p27Kip1 on IM-induced apoptosis. C Immunoblotting of cleaved caspase 9 and p27Kip1 in K562p27tet-on cells treated with IM, SenB or their combination for 24 h in the absence or presence of vehicle (-dox) or 1 µg/mL doxycycline (+dox). Exogenous p27Kip1 overexpression decreases apoptosis marker after treatment with IM, addition of SenB (I + S) increases active caspase 9 level relative to IM alone. Β-actin was used as a loading control. Statistical analysis was performed using one-way ANOVA. **p < 0.01, ****p < 0.0001. Values are mean ± SD, n = 3.

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