Fig. 5: Epigenetic regulation of FOXC1 expression in TNBC.

a ChIP-seq profiles for BRD4 in a panel of JQ1 or DMSO (vehicle control) treated breast tumor lines. b H3K27ac enrichment at TNBC-specific SEs with or without JQ1 treatment. c–e H3K27ac (c), Brd4 (d), and P300 (e) ChIP-qPCR of indicated cell lines using primer amplifying e1 of FOXC1 SE. n = 3 independent experiments. f Immunoblotting detection of FOXC1 expression in cells treated with JQ1 or DMSO, repeated independently twice with similar results. g Clonogenic growth of indicated cells with or without 0.3 µM JQ1 treatment. n = 3 independent experiments. h H3K27ac ChIP-qPCR of clinical breast cancer samples using primer amplifying e1 of FOXC1 SE. Four TNBC and four non-TNBC fresh frozen samples were tested. i Activity of constituent enhancers of FOXC1 SE measured in BT-549 cells by Dual-Luciferase reporter assay. n = 3 independent experiments. (j) Venn diagram shows TFs potentially binding to the SE region identified by prediction and mass spectrometry. The size of TFs uniquely found by prediction was proportionate to -log10 transformed p-value, and the size of TFs found by mass spectrometry only was in proportion to -log10 transformed BH-adjusted p-value. Data are represented as mean ± SEM in (c–e) and (g–i). P-values were calculated by two-sided Student’s t test in (c–e) and (g–i). Source data are provided as a Source Data file.