CK2 inhibits IKAROS-mediated repression of BCL2L1 (BCL-XL). (A-B) Effect of CK2α shRNA on mRNA levels of CK2α (A) and BC2L1 (B) in Nalm6 and 697 B-ALL cells. (C) Effect of CK2α shRNA on IKAROS binding at the BC2L1 promoter as measured by qChIP. Effect of pharmacological inhibition of CK2 (with CX-4945) on (D) BCL2L1 mRNA expression level by quantitative reverse transcription polymerase chain reaction (qRT-PCR), (E) BCL-XL protein level by western blot, and (F) IKAROS binding at the BCL2L1 promoter in Nalm6 and 697 B-ALL cells. (G-H) Effect of CX-4945 on the BCL-XL mRNA level (G) and IKAROS binding (H) at the BCL2L1 promoter in primary B-ALL cells. (I-K) Effect of CK2 overexpression (MIG-CK2) and vector only control (MIG-CTL) on BCL2L1 mRNA expression level by qRT-PCR (I), BCL-XL protein level by western blot (J), and IKAROS binding (K) at the BCL2L1 promoter in Nalm6 and 697 B-ALL cells. (L) Effect of IKZF1 knockdown (shIK) on changes in BCL2L1 gene expression induced by CK2 inhibition with CX-4945 as measured by qRT-PCR. Cells were transfected with CK2α in panels A-B or IKZF1 shRNA knockdown in panel K for 3 days using the Neon transfection method, and cells stably expressing lentiviral CK2α in panels I-J are described in the Methods section. (D-H, L) Cells were treated with 5 μM CX-4945 for 2 days. ChIP enrichments are normalized to input. Graphed in panels C, F, H, and K is the mean ± SD of 4 independent experiments. Graphed in panels A-B, D, G, I, L are the mean ± SD of triplicates representative of 1 of 3 independent experiments. *P < .05, **P < .01, ***P < .001.