a, Left, BACH1 expression levels (determined by RNA-seq) with respect to relative DNA copy-number alterations in TCGA breast cancers (n = 1105). Middle, BACH1 expression (RNA-seq) in TNBC (n = 83) or basal (n = 98) breast cancers compared to non-TNBC (n = 734) or non-basal (n = 424) breast cancers using Pam50 classification of TCGA data. Right, breast cancer subtypes classified by Pam50 (n = 522 total, n = 98 basal, n = 58 HER2-enriched, n = 231 luminal-A, n = 127 luminal-B, n = 8 normal-like). Two-tailed t-test. b, BACH1 expression levels (by RNA-seq) in patients with TNBC compared to patients that did not have TNBC, using the datasets of patients with breast cancer of METABRIC (n = 2509), GSE2034 (n = 286) and GSE11121 (n = 200). Two-tailed t-test. c, Gene Ontology terms as determined by gene set analysis for cell components that are positively correlated with BACH1 depletion based on microarray analysis of BM1-shBACH1 cell transcripts. n = 3 biologically independent samples, FDR-corrected P < 0.05. d, Left, relative mRNA levels of mitochondrial inner membrane genes in MB436-shBACH1 cells (two shBACH1 vectors, clone 1, clone 2) compared to the wild type control (MB436-shCont). Data are mean ± s.e.m., n = 3 biologically independent samples, two-tailed t-test. Right, representative western blots of mitochondrial genes using MB436-shBACH1 or control cell lysates. Each experiment was repeated independently three times with similar results. Band density quantification is shown below the blots. e, Schematic showing proximal BACH1 binding on the promoter regions of mitochondrial membrane genes. TSS, transcription start site. Arrows, primers used for ChIP-PCR. f, ChIP assays showing relative fold enrichment of BACH1 recruitment to the HMOX1 promoter using BACH1-depleted TNBC (BM1 and MB436) or control cells. g, h, ChIP assays showing fold enrichment of BACH1 and H3K27me3 recruitment to the mitochondrial membrane genes in low-BACH1-expressing MB468 and MB436 cells. For ChIP assays in f–h, data are mean ± s.e.m., n = 3 biologically independent samples, two-tailed t-test. i, KEGG pathways demonstrating the negative correlation between BACH1 expression and oxidative phosphorylation in all patients with breast cancer (n = 1,105, left) and patients with TNBC (n = 119, right). FDR values (−log 10 (FDR)) are generated in the R package GOseq using the default program Wallenius P values with Benjamini−Hochberg-corrected P values. j, Expression of ETC genes (COX15, ATP5D and ATP5G2 (also known as ATP5MC2)) in TNBC compared to tumours from patients that did not have TNBC using multiple breast cancer datasets: METABRIC (TNBC n = 319, non-TNBC n = 1661), GSE2034 (TNBC n = 54, non-TNBC n = 232) and GSE11121 (TNBC n = 33, non-TNBC n = 150). P values are determined by two-tailed t-test. k, Co-expression plots of UQCRC1 or ATP5D and BACH1 in TCGA breast cancer (n = 1105) or TNBC (n = 115) dataset. Pearson’s and Spearman’s correlation coefficients are shown. Source data