ArticleClinical epigenetics2019
The hyper-activation of transcriptional enhancers in breast cancer.
Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- A novel super-enhancer-related gene signature predicts prognosis and immune microenvironment for breast cancer.BMC cancer · 2023Trial
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- Research advances of lactylation modification in breast cancer.Discover oncology · 2025Review
- Multi-omics based and AI-driven drug repositioning for epigenetic therapy in female malignancies.Journal of translational medicine · 2025Review
- Genome-wide identification and analysis of recurring patterns of epigenetic variation across individuals.Communications biology · 2025Article
- Targeting EP300 in diffuse large b-cell lymphoma: efficacy of A485 and synergistic effects with XPO1 inhibition.BMC cancer · 2025Article
- Super-enhancer-driven EFNA1 fuels tumor progression in cervical cancer via the FOSL2-Src/AKT/STAT3 axis.The Journal of clinical investigation · 2025Article
- Chromatin Interaction and Histone Mark Signatures Associated With TBXT Expression in Metastatic Lung Cancer.Genes, chromosomes & cancer · 2025Article
- Comparative epigenomics to clinical trials in human breast cancer and canine mammary tumor.Animal cells and systems · 2025Review
- Super-enhancer DNA methylation in cancer: the mechanism of action and therapeutic directions.Frontiers in oncology · 2025Review
- Histone H4 acetylation differentially modulates proliferation in adult oligodendrocyte progenitors.The Journal of cell biology · 2024Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Cooperation of MLL1 and Jun in controlling H3K4me3 on enhancers in colorectal cancer.Genome biology · 2023Article
- Imaging-based study demonstrates how the DEK nanoscale distribution differentially correlates with epigenetic marks in a breast cancer model.Scientific reports · 2023Article
- Emerging Role of Epigenetic Modifiers in Breast Cancer Pathogenesis and Therapeutic Response.Cancers · 2023Review
- Regulation of KDM5C stability and enhancer reprogramming in breast cancer.Cell death & disease · 2022Article
- Dynamic Chromatin States Coupling with Key Transcription Factors in Colitis-Associated Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Loss of TIP60 (KAT5) abolishes H2AZ lysine 7 acetylation and causes p53, INK4A, and ARF-independent cell cycle arrest.Cell death & disease · 2022Article
- PFKM inhibits doxorubicin-induced cardiotoxicity by enhancing oxidative phosphorylation and glycolysis.Scientific reports · 2022Article
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers.Genome research · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActivation of transcription enhancers, especially super-enhancers, is one of the critical epigenetic features of tumorigenesis. However, very few studies have systematically identified the enhancers specific in cancer tissues.
methodsHere, we studied the change of histone modifications in MMTV-PyVT breast cancer model, combining mass spectrometry-based proteomics and ChIP-seq-based epigenomics approaches. Some of the proteomic results were confirmed with western blotting and IHC staining. An inhibitor of H3K27ac was applied to study its effect on cancer development.
resultsH3K27ac and H4K8ac are elevated in cancer, which was confirmed in patient tissue chips. ChIP-seq revealed that H4K8ac is co-localized with H3K27ac on chromatin, especially on distal enhancers. Epigenomic studies further identified a subgroup of super-enhancers marked by H3K4me3 peaks in the intergenic regions. The H3K4me3-enriched regions enhancers are associated with higher level of H3K27ac and H4K8ac compared with the average level of conventional super-enhancers and are associated with higher transcription level of their adjacent genes. We identified 148 H3K4me3-enriched super-enhancers with higher gene expression in tumor, which may be critical for breast cancer. One inhibitor for p300 and H3K27ac, C646, repressed tumor formation probably through inhibiting Vegfa and other genes.
conclusionsTaken together, our work identifies novel regulators and provides important resource to the genome-wide enhancer studies in breast cancer and raises the possibility of cancer treatment through modulating enhancer activity.
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