Fig. 6: Shared ER-MAF binding sites control the E2-induced metastasis gene program.

a, Enrichment of chromatin binding sites from MCF7 cells in the vicinity of E2-induced genes compared with an equal number of constitutively expressed genes in MCF7 cells. Lines illustrate the cumulative percentage of sites within a given distance from the TSSs. b, MAF/E2-shared ER-ChIP peaks that overlap with ATAC-seq peaks are enriched in the MAF/E2 condition (MAF/E2 versus mock comparison in ATAC-seq data; P < 0.10). Only one peak per gene is considered. Permutation test, two-tailed. c, Percentage of BCa ATAC-seq peaks (from TCGA⁴⁴) occupied in MCF7 cells by both MAF and ER, or only MAF or ER, that are connected to E2 target gene promoters through promoter–enhancer connections (red line). The distribution of connections between the same number of random ATAC-seq peaks and E2 target gene promoters is shown for comparison (grey); 10,000 iterations were performed to estimate the distribution to test the null hypothesis. Permutation test, one-tailed. d, Identified functional promoter–enhancer links between E2-induced genes and MAF/ER-, MAF- and ER-occupied BCa ATAC-seq peaks. e, Kaplan–Meier curves representing the probability of bone metastasis-free survival in ER⁺ BCa patients (MSKCC-EMC dataset¹³), stratified according to the expression of a MAF-dependent gene signature generated from the integration of RNA-seq transcriptomics and MAF- and MAF/E2-dependent ER ChIP-seq data. Log-rank test, two-tailed.