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. 2017 Aug 1;8(35):59476–59491. doi: 10.18632/oncotarget.19761

Figure 6. Dinaciclib or a CDK9-specific inhibitor potentiate BH3 mimetics lethality in MM cells in association with Pol II inhibition and Mcl-1 downregulation.

Figure 6

U266 and PS-R (bortezomib-resistant U266) cells (A) or RPMI8226 and H929 cells (B) were exposed (24 hr) to 500 nM ABT-737 with or without 20 μM CDK9i, followed by flow cytometry to determine the percentage of apoptotic cells *** = P < 0.001, significantly greater than values for ABT alone; ** = P < 0.01. (C) Parallel studies were performed with 100 nM alvocidib (FP) and 750 nM ABT-737. * = P < 0.05; ** = P < 0.01. Immunoblotting analysis was carried out to monitor expression of phosphorylated (serine-2 and 5, CTD) RNA pol II, Mcl-1, and PARP cleavage in U266 cells (D) and PS-R cells (E) exposed (24 hr) to the indicated concentrations of ABT-737 and CDK9i (20 μM). (F) PS-R cells were exposed to ABT ± FP for 24 hr as described in (C), after which immunoblotting analysis was carried out to monitor expression of Mcl-1 and cleavage of PARP and caspase 3 in PS-R cells.