ArticleOncogene2001
Ku antigen is required to relieve G2 arrest caused by inhibition of DNA topoisomerase II activity by the bisdioxopiperazine ICRF-193.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Catalytic inhibitors of DNA topoisomerase II suppress the androgen receptor signaling and prostate cancer progression.Oncotarget · 2015Article
- A mitotic topoisomerase II checkpoint in budding yeast is required for genome stability but acts independently of Pds1/securin.Genes & development · 2006Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ku antigen is necessary for DNA double-strand break (DSB) repair through its ability to bind DNA ends with high affinity and to recruit the catalytic subunit of DNA-PK to the DSBs. Ku-deficient cells are hypersensitive to agents causing DSBs in DNA but also to the DNA topoisomerase II (topo II) inhibitor ICRF-193, which does not induce DSBs. This suggests a new role of Ku antigen, that is independent of DSB repair by DNA-PK. Here we characterize the basis for the hypersensitivity of Ku-deficient cells to ICRF-193. Chromosome condensation and segregation, which are dependent on topo II, but also the catalytic activity of topo II in late S-G2 were inhibited to a comparable extent when ICRF-193 was applied to Ku-deficient cells or wild-type cells. However, mutant cells arrested in G2 by ICRF-193 treatment were unable to progress into M phase upon drug removal, although drug-trapped topo II complexes were removed from DNA and the two isoforms of topo II recovered their catalytic activity as in wild-type cells. The reversibility of G2 arrest was recovered by complementation of mutant cells with a human Ku86 cDNA. Notably, chromosome condensation was abnormal in Ku-deficient cells after suppression of the G2 arrest by caffeine, even in the absence of ICRF-193. These results reflect the involvement of Ku-antigen in the cellular response to topo II inhibition, more particularly in relieving G2 arrest caused by topo II inhibition in late S/G2 and the subsequent recovery of chromosome condensation.
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