Fig. 2
From: LOXL2-mediated H3K4 oxidation reduces chromatin accessibility in triple-negative breast cancer cells

H3K4ox maps to heterochromatin and controls chromatin accessibility in TNBC cells. Western blot for the indicated antibodies in a panel of breast cancer cell lines (a), TNBC cell lines (b), or PDXs (c). d Pearson correlation between two H3K4ox sequencing replicates. Distribution of all H3K4ox ChIP-seq peaks in MDA-MB-231 cells are given, with the indicated percentages. e Contingency table of the Fisher's exact test showed the statistical overrepresentation of the H3K4ox peaks through different chromatin states. f Genome browser view of H3K4ox and H3K9me3-binding profiles at two representative heterochromatin regions. g Heatmaps show the ATAC signal in all peaks as well as in peaks that overlap with H3K4ox in LOXL2 KD or control cells. h H3K4ox ChIP-PCR validation of the selected genomic regions from the ChIP-seq from control or LOXL2 KD MDA-MB-231 cells. Data of qPCR amplification were normalized to the input and to total H3 (upper panel). ATAC-qPCR validation of the incorporation of the transposase Tn5 at the selected genomic regions from the ChIP-seq from control or LOXL2 KD MDA-MB-231 cells. Data of qPCR amplification were normalized to an unchanging genomic region (the HPRT promoter) and expressed as the fold-change relative to data obtained from control cells, which were set to 1 (lower panel). In both experiments, the RNA polymerase II (POL2RA) promoter was used as a negative control. Error bars indicate the SD from at least three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001