ArticleMolecular oncology2012
Global H3K27 trimethylation and EZH2 abundance in breast tumor subtypes.
Article in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- Genetic alterations of histone lysine methyltransferases and their significance in breast cancer.Oncotarget · 2015Pooled it
- Article
- Structural characteristics and SARs of EZH2 inhibitors.Molecular diversity · 2026Review
- EZH2 directs HER2+ breast cancer progression through the modulation of epithelial plasticity.EMBO reports · 2026Article
- Epigenetic Regulation of Chromosomal Instability by EZH2 Methyltransferase.Cancer discovery · 2026Article
- Decoding Breast Cancer: Emerging Molecular Biomarkers and Novel Therapeutic Targets for Precision Medicine.International journal of molecular sciences · 2025Review
- Noncanonical association of EZH2 with E2F1 promotes tumor proliferation through chromatin remodeling.Experimental & molecular medicine · 2025Article
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- Quantitative Analysis of Nonhistone Lysine Methylation Sites and Lysine Demethylases in Breast Cancer Cell Lines.Journal of proteome research · 2025Article
- Expression patterns of H3K27me3 for differentiation of breast fibroadenomas and phyllodes tumors.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025Article
- Epigenetics and ultraviolet radiation: Implications for skin ageing and carcinogenesis.Skin health and disease · 2024Review
- Quantitative analysis of non-histone lysine methylation sites and lysine demethylases in breast cancer cell lines.bioRxiv : the preprint server for biology · 2024Article
- Menin Deficiency Induces Autism-Like Behaviors by Regulating Foxg1 Transcription and Participates in Foxg1-Related Encephalopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Epigenetic regulation of breast cancer metastasis.Cancer metastasis reviews · 2024Review
- Ezh2 promotes mammary tumor initiation through epigenetic regulation of the Wnt and mTORC1 signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Synthetic Reader-Actuators Targeted to Polycomb-Silenced Genes Block Triple-Negative Breast Cancer Proliferation and Invasion.GEN biotechnology · 2023Article
- Polycomb deficiency drives a FOXP2-high aggressive state targetable by epigenetic inhibitors.Nature communications · 2023Article
- EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis.Nature communications · 2022Article
- Review
- H3K27m3 overexpression as a new, BCL2 independent diagnostic tool in follicular and cutaneous follicle center lymphomas.Virchows Archiv : an international journal of pathology · 2022Article
40 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb repressive complex 2 (PRC2) and its core member enhancer of zeste homolog 2 (EZH2) mediate the epigenetic gene silencing mark: trimethylation of lysine 27 on histone 3 (H3K27me3). H3K27me3 is characteristic of the chromatin at genes involved in developmental regulation in undifferentiated cells. Overexpression of EZH2 has been found in several cancer types such as breast, prostate, melanoma and bladder cancer. Moreover, overexpression is associated with highly proliferative and aggressive types of breast and prostate tumors. We have analyzed the abundance of EZH2 and H3K27me3 using immunohistochemistry in two large and well-characterized breast tumor data sets encompassing more than 400 tumors. The results have been analyzed in relation to the molecular subtypes of breast tumors (basal-like, luminal A, luminal B, HER2-enriched and normal-like), as well as in subtypes defined by clinical markers (triple negative, ER+/HER2-/Ki67low, ER+/HER2-/Ki67high and HER2+), and were validated in representative breast cancer cell lines by western blot. We found significantly different expression of both EZH2 and H3K27me3 across all subtypes with high abundance of EZH2 in basal-like, triple negative and HER2-enriched tumors, and high H3K27me3 in luminal A, HER2-enriched and normal-like tumors. Intriguingly, the two markers show an inverse correlation, particularly for the basal-like and triple negative tumors. Consequently, high expression of EZH2 was associated with poor distant disease-free survival whereas high expression of H3K27me3 was associated with better survival. Additionally, none of 182 breast tumors was found to carry a previously described EZH2 mutation affecting Tyr641. Our observation that increased expression of EZH2 does not necessarily correlate with increased abundance of H3K27me3 supports the idea that EZH2 can have effects beyond epigenetic silencing of target genes in breast cancer.
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