Evidence map›Paper›PMID 25302047›Full record

ArticleMutation research2014

Oxidative stress preferentially induces a subtype of micronuclei and mediates the genomic instability caused by p53 dysfunction.

Bing Xu, Wenxing Wang, Haiyang Guo, Zhaoliang Sun, Zhao Wei, Xiyu Zhang, Zhaojian Liu, Jay A Tischfield, Yaoqin Gong, Changshun Shao

Open access · greenAbstract read
In one paragraph

Article in Mutation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  10. DNA Repair Inhibition Leads to Active Export of Repetitive Sequences to the Cytoplasm Triggering an Inflammatory Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  18. HSP90 inhibitors in the context of heat shock and the unfolded protein response: effects on a primary canine pulmonary adenocarcinoma cell line.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2017
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Bing Xu
Wenxing Wang
Haiyang Guo
Zhaoliang Sun
Zhao Wei
Xiyu Zhang
Zhaojian Liu
Jay A Tischfield
Yaoqin Gong
Changshun Shao
Shandong University · CNRutgers, The State University of New Jersey · USShandong Provincial QianFoShan Hospital · CN

Funding

Mouse Model for Chemical and Radiation MutagenesisR01ES011633 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI TISCHFIELD, JAY ARNOLD · 2002 to 2006
$1.9M
NIEHS NIH HHS R01 ES011633
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are known to cause many types of DNA lesions that could be converted into cancer-promoting genetic alterations. Evidence showed that tumor suppressor p53 plays an important role in regulating the generation of cellular ROS, either by reducing oxidative stress under physiological and mildly stressed conditions, or by promoting oxidative stress under highly stressed conditions. In this report we characterized the effect of oxidative stress on the induction of micronuclei, especially the subclass marked by pan-staining of γ-H2AX or MN-γ-H2AX (+). We found that MN-γ-H2AX (+) were more responsive to hydrogen peroxide (H2O2) than the MN-γ-H2AX (−). In human and mouse cells that are deficient in p53, the frequency of MN-γ-H2AX (+) is significantly elevated, but can be attenuated by antioxidant N-acetylcysteine (NAC). Depletion of p53-regulated antioxidant gene SESN1 by RNA interference also resulted in an elevation of MN-γ-H2AX (+). Furthermore, we found that in cells that were depleted of p400 by RNAi, and therefore were experiencing increased ROS, the frequency of MN-γ-H2AX (+), but not that of MN-γ-H2AX (−), was significantly induced. We further demonstrated that the induction of MN-γ-H2AX (+) by replication stress can also be attenuated by NAC, and that H2O2 also leads to increased phosphorylation of Chk1 and Rad17 that mimics replication stress, suggesting that replication stress and oxidative stress are intertwined and may reinforce each other in driving genomic instability. Our findings illustrate the importance of p53-regulated redox level in the maintenance of genomic stability.

Indexed as

Micronuclei, Chromosome-DefectiveAnimalsCells, CulturedDNA DamageGenomic InstabilityHEK293 CellsHistonesHumansHydrogen PeroxideMiceOxidative StressReactive Oxygen SpeciesTumor Suppressor Protein p53H2AX protein, humanHistonesHydrogen PeroxideReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID25302047
PMCPMC4186711
OpenAlexW1998555101

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.