ArticleMolecular cell2022
Multimodal regulatory elements within a hormone-specific super enhancer control a heterogeneous transcriptional response.
Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Increased chromatin accessibility following 1α,25-dihydroxyvitamin DToxicology and applied pharmacology · 2026Article
- fourSynergy: ensemble-based interaction calling on 4C-seq data using gradient-free optimization.BioData mining · 2026Article
- Understanding super enhancers in genome architecture and their roles in livestock breeding.BMC genomics · 2026Review
- Article
- Altered cofactor recruitment and nucleosome dynamics underlie bisphenol A's impact on ERα-mediated transcriptional bursting.iScience · 2025Article
- NuclampFISH enables cell sorting based on nuclear RNA expression for chromatin analysis.BMC genomics · 2025Article
- The glucocorticoid receptor potentiates aldosterone-induced transcription by the mineralocorticoid receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The enhancer RNA, AANCR, regulates APOE expression in astrocytes and microglia.Nucleic acids research · 2024Article
- Super-Enhancers and Their Parts: From Prediction Efforts to Pathognomonic Status.International journal of molecular sciences · 2024Review
- Transcriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding.Nature communications · 2023Article
- Long-range gene regulation in hormone-dependent cancer.Nature reviews. Cancer · 2023Review
- SEanalysis 2.0: a comprehensive super-enhancer regulatory network analysis tool for human and mouse.Nucleic acids research · 2023Article
- Genomic glucocorticoid action in embryonic mouse neural stem cells.Molecular and cellular endocrinology · 2023Article
- Enhancer in cancer pathogenesis and treatment.Genetics and molecular biology · 2023Article
- Exploring the potential of eRNAs in cancer immunotherapy.Molecular therapy oncolytics · 2022Article
- Glucocorticoids unmask silent non-coding genetic risk variants for common diseases.Nucleic acids research · 2022Article
- Cortisol levels in rural Latina breast cancer survivors participating in a peer-delivered cognitive-behavioral stress management intervention: TheComprehensive psychoneuroendocrinology · 2022Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The hormone-stimulated glucocorticoid receptor (GR) modulates transcription by interacting with thousands of enhancers and GR binding sites (GBSs) throughout the genome. Here, we examined the effects of GR binding on enhancer dynamics and investigated the contributions of individual GBSs to the hormone response. Hormone treatment resulted in genome-wide reorganization of the enhancer landscape in breast cancer cells. Upstream of the DDIT4 oncogene, GR bound to four sites constituting a hormone-dependent super enhancer. Three GBSs were required as hormone-dependent enhancers that differentially promoted histone acetylation, transcription frequency, and burst size. Conversely, the fourth site suppressed transcription and hormone treatment alleviated this suppression. GR binding within the super enhancer promoted a loop-switching mechanism that allowed interaction of the DDIT4 TSS with the active GBSs. The unique functions of each GR binding site contribute to hormone-induced transcriptional heterogeneity and demonstrate the potential for targeted modulation of oncogene expression.
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