ArticleGenome integrity2011
Gene amplification in human cells knocked down for RAD54.
Article in Genome integrity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- The potential clinical implications of extrachromosomal circular DNA as a biomarker.Genes & diseases · 2026Review
- Exploring the potential of extrachromosomal DNA as a novel oncogenic driver.Science China. Life sciences · 2025Review
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Extrachromosomal circular DNA: biogenesis, structure, functions and diseases.Signal transduction and targeted therapy · 2022Review
- Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.Cancer cell international · 2022Review
- Extrachromosomal circular DNA in cancer drug resistance and its potential clinical implications.Frontiers in oncology · 2022Review
- Small extrachromosomal circular DNA (eccDNA): major functions in evolution and cancer.Molecular cancer · 2021Review
- Small ring has big potential: insights into extrachromosomal DNA in cancer.Cancer cell international · 2021Review
- Review
- Current understanding of extrachromosomal circular DNA in cancer pathogenesis and therapeutic resistance.Journal of hematology & oncology · 2020Review
- Inhibiting homologous recombination decreases extrachromosomal amplification but has no effect on intrachromosomal amplification in methotrexate-resistant colon cancer cells.International journal of cancer · 2019Article
- Role of Ku70 in the apoptosis of inflamed dental pulp stem cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Sei-1 promotes double minute chromosomes formation through activation of the PI3K/Akt/BRCA1-Abraxas pathway and induces double-strand breaks in NIH-3T3 fibroblasts.Cell death & disease · 2018Article
- Rad51 and Rad54 promote noncrossover recombination between centromere repeats on the same chromatid to prevent isochromosome formation.Nucleic acids research · 2016Article
- Novel role for non-homologous end joining in the formation of double minutes in methotrexate-resistant colon cancer cells.Journal of medical genetics · 2015Article
- TERRA Expression Levels Do Not Correlate with Telomere Length and Radiation Sensitivity in Human Cancer Cell Lines.Frontiers in oncology · 2013Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn mammalian cells gene amplification is a common manifestation of genome instability promoted by DNA double-strand breaks (DSBs). The repair of DSBs mainly occurs through two mechanisms: non-homologous end-joining (NHEJ) and homologous recombination (HR). We previously showed that defects in the repair of DSBs via NHEJ could increase the frequency of gene amplification. In this paper we explored whether a single or a combined defect in DSBs repair pathways can affect gene amplification.
resultsWe constructed human cell lines in which the expression of RAD54 and/or DNA-PKcs was constitutively knocked-down by RNA interference. We analyzed their radiosensitivity and their capacity to generate amplified DNA. Our results showed that both RAD54 and DNA-PKcs deficient cells are hypersensitive to γ-irradiation and generate methotrexate resistant colonies at a higher frequency compared to the proficient cell lines. In addition, the analysis of the cytogenetic organization of the amplicons revealed that isochromosome formation is a prevalent mechanism responsible for copy number increase in RAD54 defective cells.
conclusionsDefects in the DSBs repair mechanisms can influence the organization of amplified DNA. The high frequency of isochromosome formation in cells deficient for RAD54 suggests that homologous recombination proteins might play a role in preventing rearrangements at the centromeres.
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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.