Fig. 4: FOXM1-binding CRE within BMF intronic region represses BMF while enhancing BUB1B expression.
From: FOXM1 repression increases mitotic death upon antimitotic chemotherapy through BMF upregulation
a BMF and BUB1B genomic landscape from UCSC genome browser with tracks of FOXM132 and H3K27Ac33 ChIP-seq data. b BMF promoter-reporter assay in siNeg- and siFOXM1-depleted MCF-7 cells. c BMF transcript levels in CRE#1 CRISPR/Cas9-deleted MCF-7 polyclonal cell population. d BMF transcript levels in CRE#2 CRISPR/Cas9-deleted MCF-7 polyclonal cell population. e BMF transcript levels in CRE#3 CRISPR/Cas9-deleted MCF-7 cells immediately after sorting. f BMF transcript levels in CRE#3 CRISPR/Cas9-deleted and siFOXM1-depleted MCF-7 cells immediately after sorting. g Genomic PCR validation for the ability to generate CRE#3 CRISPR/Cas9-deleted polyclonal cell population only in a BMF KO background. h Enhancer reporter assay for CRE#3 in siNeg- and siFOXM1-depleted MCF-7 cells. i BUB1B transcript levels in CRE#3 CRISPR/Cas9-deleted MCF-7 cells immediately after sorting. j 4C-seq replicates of neonatal HDFs with a viewpoint in CRE#3 (red). BMF promoter and BUB1B promoter interactions with CRE#3 are highlighted (orange). Data information: in b, f, h data are mean ± S.D. from n = 3 or n = 4 independent experiments; ****p ≤ 0.0001 (two-tailed one-way ANOVA and Tukey’s multiple comparison test). In c, d data are mean ± S.D. from n = 3 and n = 2 independent experiments; ns, p ≤ 0.05 (two-tailed Mann–Whitney test). In e, i data are mean ± S.D. from n = 4 independent experiments; *p ≤ 0.05 (two-tailed paired t test).
