Evidence map›Paper›PMID 26317544›Full record

ArticleOncotarget2015

KMT Set7/9 affects genotoxic stress response via the Mdm2 axis.

Larissa Lezina, Vasilisa Aksenova, Olga Fedorova, Daria Malikova, Oleg Shuvalov, Alexey V Antonov, Dmitri Tentler, Alexander V Garabadgiu, Gerry Melino, Nikolai A Barlev

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Arboviruses in Cancer therapy: pros and cons.Journal of neurovirology · 2026
    Review
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  4. p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
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  13. Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Review
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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 3 countries.

Larissa LezinaGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Vasilisa AksenovaGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Olga FedorovaGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Daria MalikovaGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Oleg ShuvalovGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Alexey V AntonovMRC Toxicology Unit, Leicester, LE1 9HN, UK.
Dmitri TentlerGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Alexander V GarabadgiuMolecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg, 190013, Russia.
Gerry MelinoMRC Toxicology Unit, Leicester, LE1 9HN, UK.
Nikolai A BarlevGene Expression Laboratory, Institute of Cytology, Saint-Petersburg, 194064, Russia.
Institute of Cytology · RUSt. Petersburg State Technological Institute · RUMRC Toxicology Unit · GB

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

Genotoxic stress inflicted by anti-cancer drugs causes DNA breaks and genome instability. DNA double strand breaks induced by irradiation or pharmacological inhibition of Topoisomerase II activate ATM (ataxia-telangiectasia-mutated) kinase signalling pathway that in turn triggers cell cycle arrest and DNA repair. ATM-dependent gamma-phosphorylation of histone H2Ax and other histone modifications, including ubiquitnylation, promote exchange of histones and recruitment of DNA damage response (DDR) and repair proteins. Signal transduction pathways, besides DDR itself, also control expression of genes whose products cause cell cycle arrest and/or apoptosis thus ultimately affecting the sensitivity of cells to genotoxic stress. In this study, using a number of experimental approaches we provide evidence that lysine-specific methyltransferase (KMT) Set7/9 affects DDR and DNA repair, at least in part, by regulating the expression of an E3 ubiquitin ligase, Mdm2. Furthermore, we show that Set7/9 physically interacts with Mdm2. Several cancer cell lines with inverse expression of Set7/9 and Mdm2 displayed diminished survival in response to genotoxic stress. These findings are signified by our bioinformatics studies suggesting that the unleashed expression of Mdm2 in cancer patients with diminished expression of Set7/9 is associated with poor survival outcome.

Indexed as

DNA DamageDNA RepairAntibiotics, AntineoplasticCell Line, TumorCell SurvivalComputational BiologyDatabases, GeneticDose-Response Relationship, DrugDoxorubicinGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHistonesHumansMethylnitronitrosoguanidineNeoplasmsAntibiotics, AntineoplasticDoxorubicinH2AX protein, humanHistone-Lysine N-MethyltransferaseHistonesMDM2 protein, humanMethylnitronitrosoguanidineProto-Oncogene Proteins c-mdm2SETD7 protein, humanDNA damagegenotoxic stressMdm2operettaSet7/9

Identifiers

PMID26317544
PMCPMC4694870
OpenAlexW2121861350

What OpenQuestion holds

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LicenceCC BY
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.