Chromatin modifiers – Coordinators of estrogen action

• Published in: Biomedicine & pharmacotherapy Vol. 153; p. 113548
• Main Authors: Rawłuszko-Wieczorek, Agnieszka Anna, Romanowska, Kamila, Nowicki, Michał
• Format: Journal Article
• Language: English
• Published: Elsevier Masson SAS 01.09.2022; Elsevier
• Subjects: Chromatin modifiers; Epigenetics; Estrogen; Estrogen receptors; Estrogen receptors; Epigenetics; Chromatin modifiers; Estrogen
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2022.113548

A group of hormones, called estrogens, are pivotal drivers of various physiological processes. Expectedly, estrogen-driven actions are also relevant modulators of pathophysiological changes, including cancer. Different transcriptional and tissue-specific responses are elicited mainly by two estrogen receptor (ER) isoforms, ERα and ERβ. Although perturbations of ER subtype-specific expression are correlated with clinical outcomes of cancer, the result strongly depends on co-regulators. Co-regulator acts as a ‘bridge’ that helps form large protein complexes to modulate transcriptional activity on target gene chromatin. ERs, as transcription factors, may be positively or negatively influenced by the utilisation of different tissue-specific co-regulators. These co-regulators are enzymes that create the epigenetic landscape of histone and DNA modifications, along with proteins that read these modifications and ATP-dependent chromatin remodelers. This review provides an overview and update on ER-driven responses, focusing on the complex interaction between ERs and chromatin modifiers, and discusses how chromatin accessibility and epigenetic modifications contribute to ER recruitment and transactivation. [Display omitted] •Tissue-specific ER responses strongly rely on chromatin modifiers.•Epigenetic coregulators shape specific chromatin accessibility in absence and after ligand stimulation.•The epigenetic landscape of ER binding sites altered in many diseases is often connected with therapy resistance.