ArticleMolecular oncology2010
Topoisomerase IIalpha-dependent induction of a persistent DNA damage response in response to transient etoposide exposure.
Article in Molecular oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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
22 citing papers in PubMed, 35 citations in OpenAlex.
- Stiffness-dependent alveolar type II cell senescence in idiopathic pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- Effects of Blood-Derived Products on Cellular Senescence and Inflammatory Response: A Study on Skin Rejuvenation.Current issues in molecular biology · 2024Article
- DNA Damage Response After Treatment of Cycling and Quiescent Cord Blood Hematopoietic Stem Cells With Distinct Genotoxic Noxae.Stem cells (Dayton, Ohio) · 2024Article
- Sirtuin1 meditated modification of Notch1 intracellular domain regulates nucleolar localization and activation of distinct signaling cascades.Frontiers in cell and developmental biology · 2022Article
- Doxorubicin and Aclarubicin: Shuffling Anthracycline Glycans for Improved Anticancer Agents.Journal of medicinal chemistry · 2020Article
- Biological evaluation of novel thiomaltol-based organometallic complexes as topoisomerase IIα inhibitors.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Bovine Dialyzable Leukocyte Extract IMMUNEPOTENT-CRP Induces Selective ROS-Dependent Apoptosis in T-Acute Lymphoblastic Leukemia Cell Lines.Journal of oncology · 2020Article
- Nucleolar localization of the Notch4 intracellular domain underpins its regulation of the cellular response to genotoxic stressors.Cell death discovery · 2020Article
- Nuclear rupture at sites of high curvature compromises retention of DNA repair factors.The Journal of cell biology · 2018Article
- Cell death mechanisms of the anti-cancer drug etoposide on human cardiomyocytes isolated from pluripotent stem cells.Archives of toxicology · 2018Article
- Nol12 is a multifunctional RNA binding protein at the nexus of RNA and DNA metabolism.Nucleic acids research · 2017Article
- p38 MAPK inhibits nonsense-mediated RNA decay in response to persistent DNA damage in noncycling cells.The Journal of biological chemistry · 2017Article
- miR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin.Scientific reports · 2017Article
- Review
- Physiological Roles of DNA Double-Strand Breaks.Journal of nucleic acids · 2017Review
- Virtual screening-driven repositioning of etoposide as CD44 antagonist in breast cancer cells.Oncotarget · 2016Article
- Reduced DNA double-strand break repair capacity and risk of squamous cell carcinoma of the head and neck--A case-control study.DNA repair · 2016Article
- Consequences of combining siRNA-mediated DNA methyltransferase 1 depletion with 5-aza-2'-deoxycytidine in human leukemic KG1 cells.Oncotarget · 2015Article
- Gerosuppression in confluent cells.Aging · 2014Article
- Riccardin D, a novel macrocyclic bisbibenzyl, induces apoptosis of human leukemia cells by targeting DNA topoisomerase II.Investigational new drugs · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cytotoxicity of the topoisomerase II (topoII) poison etoposide has been ascribed to the persistent covalent trapping of topoII in DNA cleavage complexes that become lethal as cells replicate their DNA. However, short term etoposide treatment also leads to subsequent cell death, suggesting that the lesions that lead to cytotoxicity arise rapidly and prior to the onset DNA replication. In the present study 1h treatment with 25muM etoposide was highly toxic and initiated a double-stranded DNA damage response as reflected by the recruitment of ATM, MDC1 and DNA-PKcs to gammaH2AX foci. While most DNA breaks were rapidly repaired upon withdrawal of the etoposide treatment, the repair machinery remained engaged in foci for at least 24h following withdrawal. TopoII siRNA ablation showed the etoposide toxicity and gammaH2AX response to correlate with the inability of the cell to correct topoIIalpha-initiated DNA damage. gammaH2AX induction was resistant to the inhibition of DNA replication and transcription, but was increased by pre-treatment with the histone deacetylase inhibitor trichostatin A. These results link the lethality of etoposide to the generation of persistent topoIIalpha-dependent DNA defects within topologically open chromatin domains.
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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.