ArticleOncogene2006
p21CDKN1A allows the repair of replication-mediated DNA double-strand breaks induced by topoisomerase I and is inactivated by the checkpoint kinase inhibitor 7-hydroxystaurosporine.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- The Development, Optimization and Future of Prime Editing.International journal of molecular sciences · 2023Review
- The Role of Genetic Polymorphisms in Differentiated Thyroid Cancer: A 2023 Update.Biomedicines · 2023Review
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- Multiplexed-Based Assessment of DNA Damage Response to Chemotherapies Using Cell Imaging Cytometry.International journal of molecular sciences · 2022Article
- Chromenopyrimidinone Controls Stemness and Malignancy by suppressing CD133 Expression in Hepatocellular Carcinoma.Cancers · 2020Article
- Transcriptional activation of p21Oncotarget · 2018Article
- Apoptotic capacity and risk of squamous cell carcinoma of the head and neck.European journal of cancer (Oxford, England : 1990) · 2017Article
- The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?International journal of molecular sciences · 2016Review
- Induction and inhibition of the pan-nuclear gamma-H2AX response in resting human peripheral blood lymphocytes after X-ray irradiation.Cell death discovery · 2016Article
- Enhanced γ-H2AX DNA damage foci detection using multimagnification and extended depth of field in imaging flow cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2015Article
- Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?Cell cycle (Georgetown, Tex.) · 2013Article
- Identification of cyclohexanone derivatives that act as catalytic inhibitors of topoisomerase I: effects on tamoxifen-resistant MCF-7 cancer cells.Investigational new drugs · 2012Article
- DNA damage response pathways and cell cycle checkpoints in colorectal cancer: current concepts and future perspectives for targeted treatment.Current cancer drug targets · 2012Review
- Multispectral imaging flow cytometry reveals distinct frequencies of γ-H2AX foci induction in DNA double strand break repair defective human cell lines.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2012Article
- Poly(ADP-ribose) polymerase inhibition enhances p53-dependent and -independent DNA damage responses induced by DNA damaging agent.Cell cycle (Georgetown, Tex.) · 2011Article
- Histone gammaH2AX and poly(ADP-ribose) as clinical pharmacodynamic biomarkers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Review
- Enhanced H2AX phosphorylation, DNA replication fork arrest, and cell death in the absence of Chk1.Molecular biology of the cell · 2010Article
- Implication of checkpoint kinase-dependent up-regulation of ribonucleotide reductase R2 in DNA damage response.The Journal of biological chemistry · 2009Article
- Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells.Nature · 2009Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
This study provides evidence for the importance of p21(CDKN1A) for the repair of replication-mediated DNA double-strand breaks (DSBs) induced by topoisomerase I. We report that defects of p21(CDKN1A) and p53 enhance camptothecin-induced histone H2AX phosphorylation (gammaH2AX), a marker for DNA DSBs. In human colon carcinoma HCT116 cells with wild-type (wt) p53, gammaH2AX reverses after camptothecin removal. By contrast, gammaH2AX increases after camptothecin removal in HCT116 cells deficient for p53 (p53-/-) or p21(CDKN1A) (p21-/-) as the cells reach the late-S and G2 phases. Since p21-/- cells exhibit similar S-phase arrest as wt cells in response to camptothecin and aphidicolin does not abrogate the enhanced gammaH2AX formation in p21-/- cells, we conclude that enhanced gammaH2AX formation in p21-/- cells is not due to re-replication. The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells. TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling) assays demonstrate that gammaH2AX formation in late S and G2 cells following CPT treatment corresponds to DNA breaks. However, these breaks are not related to apoptotic DNA fragmentation. We propose that p21(CDKN1A) prevents the collapse of replication forks damaged by stabilized topoisomerase I cleavage complexes.
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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.