ArticleOncogene2017
Identification of MYST3 as a novel epigenetic activator of ERα frequently amplified in breast cancer.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- TRERNA1-mediated acetylation represses ferroptosis of non-small cell lung cancer cells via the KAT6A/H3K23ac/TRIM24-PIK3CA pathway.Human cell · 2026Article
- Hierarchical small molecule inhibition of MYST acetyltransferases.Nature communications · 2026Article
- Beyond CDK4/6 Inhibition: Current Strategies in Hormone Receptor-Positive Metastatic Breast Cancer.Current treatment options in oncology · 2026Review
- Biological Activity and Structural Biology of Current KAT6A Inhibitor Chemotypes.Journal of medicinal chemistry · 2026Article
- Exploring KAT6 as a therapeutic target in breast cancer: epigenetic approaches for precision medicine.NPJ breast cancer · 2025Review
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Combined inhibition of KAT6A/B and Menin reverses estrogen receptor-driven gene expression programs in breast cancer.Cell reports. Medicine · 2025Article
- Hierarchical small molecule inhibition of MYST acetyltransferases.bioRxiv : the preprint server for biology · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- Cancer epigenetic therapy: recent advances, challenges, and emerging opportunities.Epigenomics · 2025Review
- Emerging opportunities to treat drug-resistant breast cancer: Discovery of novel small-molecule inhibitors against different targets.Frontiers in pharmacology · 2025Review
- Discovery and Characterization of BAY-184: A New Potent and Selective Acylsulfonamide-BenzofuranJournal of medicinal chemistry · 2024Article
- ERα status of invasive ductal breast carcinoma as a result of regulatory interactions between lysine deacetylases KAT6A and KAT6B.Scientific reports · 2024Article
- KAT6A Condensates Impair PARP1 Trapping of PARP Inhibitors in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Inhibition of lysine acetyltransferase KAT6 in ERNature medicine · 2024Article
- Emerging Role of Epigenetic Modifiers in Breast Cancer Pathogenesis and Therapeutic Response.Cancers · 2023Review
- Circular RNA Expression Signatures Provide Promising Diagnostic and Therapeutic Biomarkers for Chronic Lymphocytic Leukemia.Cancers · 2023Article
- EGCG promotes the sensory function recovery in rats after dorsal root crush injury by upregulating KAT6A and inhibiting pyroptosis.Translational neuroscience · 2023Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Estrogen receptor α (ERα) is a master driver of a vast majority of breast cancers. Breast cancer cells often develop resistance to endocrine therapy via restoration of the ERα activity through survival pathways. Thus identifying the epigenetic activator of ERα that can be targeted to block ERα gene expression is a critical topic of endocrine therapy. Here, integrative genomic analysis identified MYST3 as a potential oncogene target that is frequently amplified in breast cancer. MYST3 is involved in histone acetylation via its histone acetyltransferase domain (HAT) and, as a result, activates gene expression by altering chromatin structure. We found that MYST3 was amplified in 11% and/or overexpressed in 15% of breast tumors, and overexpression of MYST3 correlated with worse clinical outcome in estrogen receptor+ (ER+) breast cancers. Interestingly, MYST3 depletion drastically inhibited proliferation in MYST3-high, ER+ breast cancer cells, but not in benign breast epithelial cells or in MYST3-low breast cancer cells. Importantly, we discovered that knocking down MYST3 resulted in profound reduction of ERα expression, while ectopic expression of MYST3 had the reversed effect. Chromatin immunoprecipitation revealed that MYST3 binds to the proximal promoter region of ERα gene, and inactivating mutations in its HAT domain abolished its ability to regulate ERα, suggesting MYST3 functioning as a histone acetyltransferase that activates ERα promoter. Furthermore, MYST3 inhibition with inducible MYST3 shRNAs potently attenuated breast tumor growth in mice. Together, this study identifies the first histone acetyltransferase that activates ERα expression which may be potentially targeted to block ERα at transcriptional level.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.