ArticleCell reports2019
Activation of Oncogenic Super-Enhancers Is Coupled with DNA Repair by RAD51.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- The breakome of BRCA1 and BRCA2 pathway mutation carriers reveals early processes in breast oncogenesis.Cell death & disease · 2025Article
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
- Human papillomavirus genomes associate with active host chromatin during persistent viral infection.PLoS pathogens · 2025Article
- ChromInSight: Revealing DNA Double-Strand Breaks Through Chromatin Structural Insights With an Interpretable Graph Neural Network Framework.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TEAD-targeting small molecules induce a cofactor switch to regulate the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ligand-specific regulation of a binary enhancer code dictating cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- YAP controls cell migration and invasion through a Rho GTPase switch.Science signaling · 2025Article
- Human Papillomavirus Genomes Associate with Active Host Chromatin during Persistent Viral Infection.bioRxiv : the preprint server for biology · 2025Article
- FOXM1 expression reverts aging chromatin profiles through repression of the senescence-associated pioneer factor AP-1.Nature communications · 2025Article
- Recent Advances in Pineoblastoma Research: Molecular Classification, Modelling and Targetable Vulnerabilities.Cancers · 2025Review
- Liquid-liquid phase separation in super enhancer-driven oncogenesis: mechanisms, immune evasion, and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Precise Mapping of Physiological DSBs Using In-Suspension Break Labeling In Situ and Sequencing (sBLISS).Methods in molecular biology (Clifton, N.J.) · 2025Article
- RAD51 regulates eukaryotic chromatin motions in the absence of DNA damage.Molecular biology of the cell · 2024Article
- Supervised learning of enhancer-promoter specificity based on genome-wide perturbation studies highlights areas for improvement in learning.Bioinformatics (Oxford, England) · 2024Article
- Stratifying TAD boundaries pinpoints focal genomic regions of regulation, damage, and repair.Briefings in bioinformatics · 2024Article
- TOP1 and R-loops facilitate transcriptional DSBs at hypertranscribed cancer driver genes.iScience · 2024Article
- Pharmacological modulation of RB1 activity mitigates resistance to neoadjuvant chemotherapy in locally advanced rectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Leveraging Tissue-Specific Enhancer-Target Gene Regulatory Networks Identifies Enhancer Somatic Mutations That Functionally Impact Lung Cancer.Cancer research · 2024Article
- Targeting super-enhancer activity for colorectal cancer therapy.American journal of translational research · 2024Review
- TDP1 suppresses chromosomal translocations and cell death induced by abortive TOP1 activity during gene transcription.Nature communications · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are deleterious and tumorigenic but could also be essential for DNA-based processes. Yet the landscape of physiological DSBs and their role and repair are still elusive. Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcription-coupled repair mechanism at oncogenic super-enhancers. At these super-enhancers the transcription factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway. Depletion of TEAD4 or RAD51 increases DSBs at RAD51/TEAD4 common binding sites within super-enhancers and decreases expression of related genes, which are mostly oncogenes. Co-localization of RAD51 with transcription factors at super-enhancers occurs in various cell types, suggesting a broad phenomenon. Together, our findings uncover a coupling between transcription and repair mechanisms at oncogenic super-enhancers, to control the hyper-transcription of multiple cancer drivers.
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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.