ArticleThe EMBO journal2021
CTCF binding modulates UV damage formation to promote mutation hot spots in melanoma.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 33 citations in OpenAlex.
- Widespread atypical UV-induced mutations form in single-stranded DNA.Science advances · 2026Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.Nucleic acids research · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Nature communications · 2026Article
- Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.International journal of radiation biology · 2026Review
- A Targetable Developmental Program Coregulates Angiogenesis and Immune Evasion in Melanoma.Cancer discovery · 2026Article
- Altered benzo[a]pyrene adduct formation in nucleosomes establishes distinct mutational patterns in lung cancer.The Journal of biological chemistry · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.bioRxiv : the preprint server for biology · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- LncRNA NEAT1 restrains the malignant biological characteristics of acute myeloid leukemia via regulating CTCF/CXCR2 axis.Clinical and experimental medicine · 2025Article
- Mapping transcription factor binding sites by learning UV damage fingerprints.Nucleic acids research · 2025Article
- Genome-wide maps of UV damage repair and mutation suppression by CPD photolyase.Nucleic acids research · 2025Article
- The epigenetic landscape shapes smoking-induced mutagenesis by modulating DNA damage susceptibility and repair efficiency.Nucleic acids research · 2025Article
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Methods and applications of genome-wide profiling of DNA damage and rare mutations.Nature reviews. Genetics · 2024Review
- Ultraviolet (UV) radiation: a double-edged sword in cancer development and therapy.Molecular biomedicine · 2024Review
- ASH1L guards cis-regulatory elements against cyclobutane pyrimidine dimer induction.Nucleic acids research · 2024Article
- Hidden secrets of the cancer genome: unlocking the impact of non-coding mutations in gene regulatory elements.Cellular and molecular life sciences : CMLS · 2024Review
- 3C methods in cancer research: recent advances and future prospects.Experimental & molecular medicine · 2024Review
- Genome-wide impact of cytosine methylation and DNA sequence context on UV-induced CPD formation.Environmental and molecular mutagenesis · 2024Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Somatic mutations in DNA-binding sites for CCCTC-binding factor (CTCF) are significantly elevated in many cancers. Prior analysis has suggested that elevated mutation rates at CTCF-binding sites in skin cancers are a consequence of the CTCF-cohesin complex inhibiting repair of UV damage. Here, we show that CTCF binding modulates the formation of UV damage to induce mutation hot spots. Analysis of genome-wide CPD-seq data in UV-irradiated human cells indicates that formation of UV-induced cyclobutane pyrimidine dimers (CPDs) is primarily suppressed by CTCF binding but elevated at specific locations within the CTCF motif. Locations of CPD hot spots in the CTCF-binding motif coincide with mutation hot spots in melanoma. A similar pattern of damage formation is observed at CTCF-binding sites in vitro, indicating that UV damage modulation is a direct consequence of CTCF binding. We show that CTCF interacts with binding sites containing UV damage and inhibits repair by a model repair enzyme in vitro. Structural analysis and molecular dynamic simulations reveal the molecular mechanism for how CTCF binding modulates CPD formation.
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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.