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Breast cancer identity is defined by specialized enhancer sets via lysine deacetylation

Tachiwana, H.; Kumegawa, K.; Matsudo, R.; Katsuma, A.; Okabe, A.; Yoshida, N.; Shu, X.; Kato, M.; Minamisawa, T.; Ito, A.; Kimura, H.; Carninci, P.; Kaneda, A.; Daigaku, Y.; Maruyama, R.; Saitoh, N.

2025-08-02 cancer biology
10.1101/2025.07.31.668008 bioRxiv
Show abstract

Breast cancer subtypes are defined by distinct transcriptional programs, yet the epigenetic mechanisms underlying subtype-specific gene regulation remain unclear. Enhancers, key regulators of gene expression and cell identity, are well positioned to define breast cancer subtypes. Here, we identify a previously unrecognized class of enhancers, termed hypoacetylation-defined (HD) enhancers, that regulate cancer-related genes in a luminal breast cancer cell line. HD enhancers are defined by RNA polymerase II dissociation upon lysine deacetylase inhibition, and bidirectional eRNA transcription. They are distinct from super-enhancers, require a specific Mediator subunit for gene-specific transcription, and form extensive chromatin interactions suggestive of a hub-like architecture. Analyses of clinical datasets further identified a subset of HD enhancers, termed HD cluster 1 enhancers, which classify patients into breast cancer subtypes and are associated with expression quantitative trait loci linked to subtype-specific gene expression. This study identifies the lysine deacetylation-regulated cell identity enhancers, which are potential therapeutic targets.

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