ArticleChromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology2015
Progression of chromosomal damage induced by etoposide in G2 phase in a DNA-PKcs-deficient context.
Article in Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- PD-1/PD-L1 and DNA Damage Response in Cancer.Cells · 2023Review
- Article
- Inhibition of DNA-PK potentiates the synergistic effect of NK314 and etoposide combination on human glioblastoma cells.Molecular biology reports · 2020Article
- Overexpression of the base excision repair NTHL1 glycosylase causes genomic instability and early cellular hallmarks of cancer.Nucleic acids research · 2018Article
- Cancer cells that survive checkpoint adaptation contain micronuclei that harbor damaged DNA.Cell cycle (Georgetown, Tex.) · 2016Article
- Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics.Journal of visualized experiments : JoVE · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Etoposide (ETO), a drug used for the treatment of human tumors, is associated with the development of secondary malignancies. Recently, therapeutic strategies have incorporated chemosensitizing agents to improve the tumoral response to this drug. ETO creates DNA double-strand breaks (DSB) via inhibition of DNA topoisomerase II (Top2). To repair DSB, homologous recombination (HR) and non-homologous end-joining (NHEJ), involving D-NHEJ (dependent of the catalytic subunit of DNA-dependent protein kinase, DNA-PKcs) and B-NHEJ (backup repair pathway) are activated. We evaluated the progression of the DNA damage induced by the Top2 poison ETO in G2 phase of human HeLa cells after chemical inhibition of DNA-PKcs with NU7026. Compared to ETO treatment alone, this combined treatment resulted in a twofold higher rate of chromatid breaks and exchanges when analysis was performed in the following metaphase. Moreover, when analysis was performed in the second metaphase following treatment, increases in the percentage of micronuclei with H2AX (biomarker for DSB) foci in binucleated cells and dicentric chromosomes were seen. In post-mitotic G1 phase, a close association between unresolved DSB and meiotic recombination 11 homolog A (MRE11) signals was observed, demonstrating the contribution of MRE11 in the DSB repair by B-NHEJ. Hence, chemical inhibition of DNA-PKcs impaired both D-NHEJ and HR repair pathways, altering the maintenance of chromosomal integrity and cell proliferation. Our results suggest that the chemosensitizing effectiveness of the DNA-PKcs inhibitor and the survival rate of aberrant cells may contribute to the development of therapy-related tumors.
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