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. 2021 Mar 5;13(5):1127. doi: 10.3390/cancers13051127

Figure 4.

Figure 4

CK2 inhibitor increases IKAROS DNA-binding to BCL-XL. Chromatin immunoprecipitation (ChIP) followed by next-generation sequencing (ChIP-seq) and analysis of genome-wide occupancy of IKAROS was performed on U937 following the CX-4945 treatment at 10 µM concentration for 72 h. A change in IKAROS binding to promoter regions of the BCL-XL gene was analyzed following the CX-4945 treatment. (A) A chIP-seq signal map for IKAROS binding to the BCL-XL/BCL-2L1 promoter region in U937-untreated labeled as WT (wild-type) (top panel) and CX-4945 treated U937 (bottom panel). Y-axis represents the log-2-fold change enrichment of IKAROS binding (** p < 0.01). (B) U937 and primary AML cells (AML-1) cells were treated with 10 and 5 μM of CX-4945, respectively (based on the IC50 value) for 48 and 72 h. IKAROS binding to the BCL-XL promoter region was confirmed using the qChIP assay in WT and CX-4945 treated cells. Binding at 72 h was not significantly increased compared to the 48 h treatment (not shown in the graph). Results are the mean +/– SD of three independent experiments. P-value summaries are as follows: p > 0.05 (ns-non significant); p < 0.001 (***); p < 0.0001 (****).