ArticleCell cycle (Georgetown, Tex.)2018
Inherited DNA lesions determine G1 duration in the next cell cycle.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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55 citing papers in PubMed.
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- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Probabilistic modeling of cell cycle dynamics in response to cell cycle targeting chemotherapy drugs to guide treatment strategies.PLoS computational biology · 2025Article
- Piceatannol and Pumpkin Seed Oil Synergistically Promote Apoptosis of PC3 Prostate Cancer Cells via Intrinsic Mitochondrial Pathway.ACS omega · 2025Article
- Targeting Mitochondrial Reactive Oxygen Species: JP4-039's Potential as a Cardiovascular Therapeutic.Journal of clinical medicine · 2025Review
- ACSL5 regulated acetyl-CoA to promote bladder cancer cellular senescence via 53BP1 acetylation.Oncogene · 2025Article
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- hTERT and SV40LgT Renal Cell Lines Adjust Their Transcriptional Responses After Copy Number Changes from the Parent Proximal Tubule Cells.International journal of molecular sciences · 2025Article
- Pro-survival roles for p21(Cip1/Waf1) in non-small cell lung cancer.British journal of cancer · 2025Article
- Research on biliary atresia and epigenetic factors from the perspective of transcriptomics: identification of key genes and experimental validation.Frontiers in pediatrics · 2025Article
- Onco-therapeutic Effect of Novel Triterpenoid Compound Oleanolic Acid Isolated and Characterized from the Methanolic Extract of Coldenia procumbens (Linn.).Applied biochemistry and biotechnology · 2024Article
- GCN2-SLC7A11 axis coordinates autophagy, cell cycle and apoptosis and regulates cell growth in retinoblastoma upon arginine deprivation.Cancer & metabolism · 2024Article
- BRCA1 and 53BP1 regulate reprogramming efficiency by mediating DNA repair pathway choice at replication-associated double-strand breaks.Cell reports · 2024Article
- Development of Daruharidra (Current pharmaceutical biotechnology · 2024Article
- Andrographolide nanophytosomes exhibit enhanced cellular delivery and pro-apoptotic activities in HepG2 liver cancer cells.Drug delivery · 2023Article
- Nano-Architecture of Persistent Focal DNA Damage Regions in the Minipig Epidermis Weeks after Acute γ-Irradiation.Biomolecules · 2023Article
- Article
- The Potential of Glucose Treatment to Reduce Reactive Oxygen Species Production and Apoptosis of Inflamed Neural Cells In Vitro.Biomedicines · 2023Article
- New 1,3,4-thiadiazoles as potential anticancer agents: pro-apoptotic, cell cycle arrest, molecular modelling, and ADMET profile.RSC advances · 2023Article
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Abstract
Replication stress is a major source of DNA damage and an important driver of cancer development. Replication intermediates that occur upon mild forms of replication stress frequently escape cell cycle checkpoints and can be transmitted through mitosis into the next cell cycle. The consequences of such inherited DNA lesions for cell fate and survival are poorly understood. By using time-lapse microscopy and quantitative image-based cytometry to simultaneously monitor inherited DNA lesions marked by the genome caretaker protein 53BP1 and cell cycle progression, we show that inheritance of 53BP1-marked lesions from the previous S-phase is associated with a prolonged G1 duration in the next cell cycle. These results suggest that cell-to-cell variation in S-phase commitment is determined, at least partially, by the amount of replication-born inherited DNA damage in individual cells. We further show that loss of the tumor suppressor protein p53 overrides replication stress-induced G1 prolongation and allows S-phase entry with excessive amounts of inherited DNA lesions. Thus, replication stress and p53 loss may synergize during cancer development by promoting cell cycle re-entry with unrepaired mutagenic DNA lesions originating from the previous cell cycle.
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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 Socratic graph.