ArticleNature communications2016
Defective DNA single-strand break repair is responsible for senescence and neoplastic escape of epithelial cells.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- PARP1 Suppression Drives ROS Resistance in Aneuploid Cancer Cells.bioRxiv : the preprint server for biology · 2026Article
- A Review of Ionizing Radiation-Induced Senescence of Bone Marrow Mesenchymal Stem/Stromal Cells: Mechanisms and Therapeutic Strategies.Current issues in molecular biology · 2026Review
- Article
- Targeting ATF6α Attenuates UVB-Induced Senescence and Improves Skin Homeostasis by Regulating IL8 Expression.Aging cell · 2025Article
- Senescence in the ageing skin: a new focus on mTORC1 and the lysosome.The FEBS journal · 2025Review
- Article
- Decoding the mechanisms behind second primary cancers.Journal of translational medicine · 2025Review
- Review
- Review
- Prostaglandin EAging · 2024Article
- Distinct regulation of ATM signaling by DNA single-strand breaks and APE1.Nature communications · 2024Article
- Therapy-induced senescence through the redox lens.Redox biology · 2024Review
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Intervention treatment reducing cellular senescence inhibits tubulointerstitial fibrosis in diabetic mice following acute kidney injury.Clinical science (London, England : 1979) · 2024Article
- Unravelling the molecular basis of PARP inhibitor resistance in prostate cancer with homologous recombination repair deficiency.International review of cell and molecular biology · 2024Review
- c-Jun N-terminal kinase signaling in cellular senescence.Archives of toxicology · 2023Review
- Epigenetic Iinsights into the Senescence of Porcine Fetal Fibroblasts induced by Passaging.Cell cycle (Georgetown, Tex.) · 2023Article
- A novel multifunctional radioprotective strategy using P7C3 as a countermeasure against ionizing radiation-induced bone loss.Bone research · 2023Article
- Flow Cytometry-based Method for Efficient Sorting of Senescent Cells.Bio-protocol · 2023Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main characteristic of senescence is its stability which relies on the persistence of DNA damage. We show that unlike fibroblasts, senescent epithelial cells do not activate an ATM-or ATR-dependent DNA damage response (DDR), but accumulate oxidative-stress-induced DNA single-strand breaks (SSBs). These breaks remain unrepaired because of a decrease in PARP1 expression and activity. This leads to the formation of abnormally large and persistent XRCC1 foci that engage a signalling cascade involving the p38MAPK and leading to p16 upregulation and cell cycle arrest. Importantly, the default in SSB repair also leads to the emergence of post-senescent transformed and mutated precancerous cells. In human-aged skin, XRCC1 foci accumulate in the epidermal cells in correlation with a decline of PARP1, whereas DDR foci accumulate mainly in dermal fibroblasts. These findings point SSBs as a DNA damage encountered by epithelial cells with aging which could fuel the very first steps of carcinogenesis.
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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.