ArticleJournal of cellular physiology2014
Link between DNA damage and centriole disengagement/reduplication in untransformed human cells.
Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 38 citations in OpenAlex.
- M phase-specific generation of supernumerary centrioles in cancer cells.Molecular biology of the cell · 2025Article
- PLK4 as a potential target to enhance radiosensitivity in triple-negative breast cancer.Radiation oncology (London, England) · 2024Article
- Mild replication stress causes premature centriole disengagement via a sub-critical Plk1 activity under the control of ATR-Chk1.Nature communications · 2023Article
- Hornerin mediates phosphorylation of the polo-box domain in Plk1 by Chk1 to induce death in mitosis.Cell death and differentiation · 2023Article
- Expanding roles of centrosome abnormalities in cancers.BMB reports · 2023Review
- The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?Frontiers in cell and developmental biology · 2023Review
- BRCA1 transports the DNA damage signal for CDDP-induced centrosome amplification through the centrosomal Aurora A.Cancer science · 2022Article
- Article
- Mind the replication gap.Royal Society open science · 2021Review
- Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021Review
- Cep57 and Cep57L1 maintain centriole engagement in interphase to ensure centriole duplication cycle.The Journal of cell biology · 2021Article
- Review
- Mild replication stress causes chromosome mis-segregation via premature centriole disengagement.Nature communications · 2019Article
- The Emerging Link between Centrosome Aberrations and Metastasis.Developmental cell · 2019Review
- Once and only once: mechanisms of centriole duplication and their deregulation in disease.Nature reviews. Molecular cell biology · 2018Review
- Building the right centriole for each cell type.The Journal of cell biology · 2018Review
- Centriole splitting caused by loss of the centrosomal linker protein C-NAP1 reduces centriolar satellite density and impedes centrosome amplification.Molecular biology of the cell · 2017Article
- Opposing post-translational modifications regulate Cep76 function to suppress centriole amplification.Oncogene · 2016Article
- PCM1 Depletion Inhibits Glioblastoma Cell Ciliogenesis and Increases Cell Death and Sensitivity to Temozolomide.Translational oncology · 2016Article
- Centrosomes in the DNA damage response--the hub outside the centre.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The radiation and radiomimetic drugs used to treat human tumors damage DNA in both cancer cells and normal proliferating cells. Centrosome amplification after DNA damage is well established for transformed cell types but is sparsely reported and not fully understood in untransformed cells. We characterize centriole behavior after DNA damage in synchronized untransformed human cells. One hour treatment of S phase cells with the radiomimetic drug, Doxorubicin, prolongs G2 by at least 72 h, though 14% of the cells eventually go through mitosis in that time. By 72 h after DNA damage we observe a 52% incidence of centriole disengagement plus a 10% incidence of extra centrioles. We find that either APC/C or Plk activities can disengage centrioles after DNA damage, though they normally work in concert. All disengaged centrioles are associated with γ-tubulin and maturation markers and thus, should in principle be capable of reduplicating and organizing spindle poles. The low incidence of reduplication of disengaged centrioles during G2 is due to the p53-dependent expression of p21 and the consequent loss of Cdk2 activity. We find that 26% of the cells going through mitosis after DNA damage contain disengaged or extra centrioles. This could produce genomic instability through transient or persistent spindle multipolarity. Thus, for cancer patients the use of DNA damaging therapies raises the chances of genomic instability and evolution of transformed characteristics in proliferating normal cell populations.
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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 Socratic graph.