Inhibition of cBAF activity hampers RUNX1 binding to the CXCR4 enhancers and downregulates CXCR4 expression. (A-B) Cell surface CXCR4 expression (A) and migration activity (B) of the indicated knockout Jurkat cells. Expression was determined by flow cytometry. Cells expressing gAAVS1 were used as a control. Data are shown as mean ± SD (n = 3). (C) ATAC-seq and ChIP-seq data in a 35-kb region including CXCR4 enhancer regions (SE [intron 1], E1 [−13.5 kb], E2 [−16.2 kb], E3 [−18.1 kb], and E4 [−18.6 kb]) and an NR3C1 motif (see “Discussion”). (D-E) Cell surface expression of CXCR4 (D) and migration activity (E) of Jurkat cells in which the indicated RUNX1 binding sites were disrupted by the CRISPR-Cas9 technology. Data are shown as mean ± SD (n = 3). E1 disruption also significantly decreased CXCR4 expression but the change was negligible (D). (F-H) ChIP-qPCR analysis of RUNX1 (F, H) and H3K27ac (G) at the CXCR4 SE and E4 enhancers in the indicated knockout Jurkat cells (F, G) and Jurkat cells treated with DMSO and BRM014 at 1 μM for 6 hours (H). The CTCF binding element 9-kb upstream of SMARCC1 was used as a control region. Data are shown as mean ± SD (n = 3-4). Two-tailed Student t test was used to assess statistical significance in panels A, B, D, E, F, G, and H (∗∗∗P < .001; ∗∗P < .01; ∗P < .05). DMSO, dimethyl sulfoxide; qPCR, quantitative polymerase chain reaction; SD, standard deviation.