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. Author manuscript; available in PMC: 2017 Jun 19.
Published in final edited form as: Oncogene. 2016 Dec 19;36(23):3263–3273. doi: 10.1038/onc.2016.471

Figure 5. Dinaciclib inhibits RALB activation and has RALB-dependent anti-leukemic effects in human AML cell lines.

Figure 5

(a) Western blot for RALB-GTP, total RALB, and GAPDH proteins in KG1 AML cells treated for 8 hours with DMSO or dinaciclib (representative of 3 independent experiments). (b) Phosphorylated TBK1 (pTBK1) levels in AML cells 24 hours after treatment with dinaciclib (representative of 3 independent experiments). (c) Percentage of AML cells with cleaved PARP (cPARP+) (top) and proportion of G0/G1 cells (bottom) 24 hours after treatment with dinaciclib determined by flow cytometry (n = 3 independent experiments, error bars = standard error of the mean, * P < 0.05). (d) MTS viability analysis of AML cell lines 72 hours after dinaciclib treatment and calculated half-maximal inhibitory concentrations (IC50)(n = 3-5 independent experiments, error bars are not included for clarity of presentation and are included in Supplemental Figure 4). (e) Relative leukemic colony formation (L-CFC) of THP1 transduced with RALB(Q72L), myristoylated AKT (myrAKT), CRAF 22W, or control vector (BFP) 24 hours after treatment with dinaciclib relative to DMSO treated controls (n = 3 independent experiments, error bars = 1 standard deviation, * P < 0.05).