ArticleProceedings of the National Academy of Sciences of the United States of America2020
Topoisomerase I-driven repair of UV-induced damage in NER-deficient cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Microbial Natural Products Targeting theMicroorganisms · 2026Review
- Two Faces of UV Mutagenesis: Independent and Collateral Mutagenesis in Skin Cancers.Life (Basel, Switzerland) · 2026Article
- Study of inborn errors of immunity associated lymphoid proliferations identifies association of presence of somatic variations with large cell morphology, copy number alterations in TNFAIP3 and heterozygous variants in EMSY.Virchows Archiv : an international journal of pathology · 2026Article
- Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms.Cell death discovery · 2025Article
- Camptothecin, a topoisomerase I inhibitor, impedes productive herpes simplex virus type 1 infection.Journal of virology · 2025Article
- Novel role of general transcript factor IIH subunit 2 (GTF2H2) in the development and sex disparity of hepatocellular carcinoma.Oncogene · 2025Article
- Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging, mismatch repair deficiency and temozolomide chemotherapy.Nucleic acids research · 2025Article
- The inherent defects of cold atmospheric plasma for the treatment of burns.Frontiers in pharmacology · 2025Article
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- PARP1-driven repair of topoisomerase IIIα DNA-protein crosslinks by FEN1.Cell reports · 2024Article
- Cross-species investigation into the requirement of XPA for nucleotide excision repair.Nucleic acids research · 2024Article
- Molecular Dynamics Investigations of Human DNA-Topoisomerase I Interacting with Novel Dewar Valence Photo-Adducts: Insights into Inhibitory Activity.International journal of molecular sciences · 2023Article
- Experimental systems for the analysis of mutational signatures: no 'one-size-fits-all' solution.Biochemical Society transactions · 2023Article
- Article
- DNA Repair Deficiency Regulates Immunity Response in Cancers: Molecular Mechanism and Approaches for Combining Immunotherapy.Cancers · 2023Review
- Human topoisomerases and their roles in genome stability and organization.Nature reviews. Molecular cell biology · 2022Review
- XRCC1 counteracts poly(ADP ribose)polymerase (PARP) poisons, olaparib and talazoparib, and a clinical alkylating agent, temozolomide, by promoting the removal of trapped PARP1 from broken DNA.Genes to cells : devoted to molecular & cellular mechanisms · 2022Article
- Lignin Nanoparticles Deliver Novel Thymine Biomimetic Photo-Adducts with Antimelanoma Activity.International journal of molecular sciences · 2022Article
- Unravelling the instability of mutational signatures extractionFrontiers in genetics · 2022Article
- Replication-dependent cytotoxicity and Spartan-mediated repair of trapped PARP1-DNA complexes.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Nucleotide excision repair (NER) removes helix-destabilizing adducts including ultraviolet (UV) lesions, cyclobutane pyrimidine dimers (CPDs), and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). In comparison with CPDs, 6-4PPs have greater cytotoxicity and more strongly destabilizing properties of the DNA helix. It is generally believed that NER is the only DNA repair pathway that removes the UV lesions as evidenced by the previous data since no repair of UV lesions was detected in NER-deficient skin fibroblasts. Topoisomerase I (TOP1) constantly creates transient single-strand breaks (SSBs) releasing the torsional stress in genomic duplex DNA. Stalled TOP1-SSB complexes can form near DNA lesions including abasic sites and ribonucleotides embedded in chromosomal DNA. Here we show that base excision repair (BER) increases cellular tolerance to UV independently of NER in cancer cells. UV lesions irreversibly trap stable TOP1-SSB complexes near the UV damage in NER-deficient cells, and the resulting SSBs activate BER. Biochemical experiments show that 6-4PPs efficiently induce stable TOP1-SSB complexes, and the long-patch repair synthesis of BER removes 6-4PPs downstream of the SSB. Furthermore, NER-deficient cancer cell lines remove 6-4PPs within 24 h, but not CPDs, and the removal correlates with TOP1 expression. NER-deficient skin fibroblasts weakly express TOP1 and show no detectable repair of 6-4PPs. Remarkably, the ectopic expression of TOP1 in these fibroblasts led them to completely repair 6-4PPs within 24 h. In conclusion, we reveal a DNA repair pathway initiated by TOP1, which significantly contributes to cellular tolerance to UV-induced lesions particularly in malignant cancer cells overexpressing TOP1.
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