ArticleNucleic acids research2014
Establishment of active chromatin structure at enhancer elements by mixed-lineage leukemia 1 to initiate estrogen-dependent gene expression.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- FOXA2 as a SETD1A-Regulated Driver of Tamoxifen Resistance in Breast Cancer.Oncology research · 2026Article
- How histone modifications influence cellular radiosensitivity: Pharmaceutically targeting epigenetic regulators as a promising avenue to overcome radioresistance.Acta pharmaceutica Sinica. B · 2025Review
- DNA Methylation Status of Regulatory Regions of Apoptosis-Associated Genes in Dystropy «Huntington's Disease-Non-Small Cell Lung Cancer».Epigenomes · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin-MLL Inhibition.Cancer discovery · 2023Article
- Partitioned usage of chromatin remodelers by nucleosome-displacing factors.Cell reports · 2022Article
- PHF20 is crucial for epigenetic control of starvation-induced autophagy through enhancer activation.Nucleic acids research · 2022Article
- Histone modification and histone modification-targeted anti-cancer drugs in breast cancer: Fundamentals and beyond.Frontiers in pharmacology · 2022Review
- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
- SETD1A Promotes Proliferation of Castration-Resistant Prostate Cancer Cells via FOXM1 Transcription.Cancers · 2020Article
- Histone methyltransferases regulate the transcriptional expression of ERα and the proliferation of tamoxifen-resistant breast cancer cells.Breast cancer research and treatment · 2020Article
- Isolation of MLL1 Inhibitory RNA Aptamers.Biomolecules & therapeutics · 2019Article
- Aberrant expression of SETD1A promotes survival and migration of estrogen receptor α-positive breast cancer cells.International journal of cancer · 2018Article
- Enhancer DNA methylation in acute myeloid leukemia and myelodysplastic syndromes.Cellular and molecular life sciences : CMLS · 2018Review
- Cytosine modifications modulate the chromatin architecture of transcriptional enhancers.Genome research · 2017Article
- Single-cell profiling reveals that eRNA accumulation at enhancer-promoter loops is not required to sustain transcription.Nucleic acids research · 2017Article
- Crosstalk between Aryl Hydrocarbon Receptor and Glucocorticoid Receptor in Human Retinal Pigment Epithelial Cells.International journal of endocrinology · 2017Article
- Changes in Gene Expression and Estrogen Receptor Cistrome in Mouse Liver Upon Acute E2 Treatment.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Cell-specific expression ofInternational journal of immunopathology and pharmacologyArticle
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
A number of genome-wide analyses have revealed that estrogen receptor α binding to and regulation of its target genes correlate with binding of FOXA1, a pioneer factor, to nearby DNA sites in MCF-7 breast cancer cells. The enhancer element-specific histone H3K4me1/2 mark is enriched at the specific FOXA1/ERα recruitment sites in chromatin, but the mechanism by which these enhancer marks are established in chromatin before hormone treatment is unclear. Here, we show that mixed-lineage leukemia 1 (MLL1) protein is a key determinant that maintains permissive chromatin structure of the TFF1 enhancer region. MLL1 occupies the TFF1 enhancer region and methylates H3K4 before hormone stimulation. In vitro, MLL1 binds directly to the CpG-rich region of the TFF1 enhancer, and its binding is dependent on hypomethylation of DNA. Furthermore, the depletion of MLL1 in MCF-7 cells results in a dramatic decrease of chromatin accessibility and recruitment of FOXA1 and ERα to the enhancer element. Our study defines the mechanism by which MLL1 nucleates histone H3K4 methylation marks in CpG-enriched regions to maintain permissive chromatin architecture and allow FOXA1 and estrogen receptor α binding to transcriptional regulatory sites in breast cancer cells.
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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.