Evidence map›Paper›PMID 28843151›Full record

ArticleRedox biology2018

Reduced levels of methyltransferase DNMT2 sensitize human fibroblasts to oxidative stress and DNA damage that is accompanied by changes in proliferation-related miRNA expression.

Anna Lewinska, Jagoda Adamczyk-Grochala, Ewa Kwasniewicz, Anna Deregowska, Ewelina Semik, Tomasz Zabek, Maciej Wnuk

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 87 citations in OpenAlex.

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  17. Longevity, Centenarians and Modified Cellular Proteodynamics.International journal of molecular sciences · 2023
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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

7 authors at 2 institutions in 1 country.

Anna LewinskaLaboratory of Cell Biology, University of Rzeszow, Pigonia 1, 35-310 Rzeszow, Poland. Electronic address: lewinska@ur.edu.pl.
Jagoda Adamczyk-GrochalaLaboratory of Cell Biology, University of Rzeszow, Pigonia 1, 35-310 Rzeszow, Poland.
Ewa KwasniewiczLaboratory of Cell Biology, University of Rzeszow, Pigonia 1, 35-310 Rzeszow, Poland.
Anna DeregowskaPostgraduate School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland; Department of Genetics, University of Rzeszow, Rzeszow, Poland.
Ewelina SemikLaboratory of Genomics, National Research Institute of Animal Production, Balice n. Cracow, Poland.
Tomasz ZabekLaboratory of Genomics, National Research Institute of Animal Production, Balice n. Cracow, Poland.
Maciej WnukDepartment of Genetics, University of Rzeszow, Rzeszow, Poland.
Rzeszów University · PLNational Research Institute of Animal Production · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methyltransferase DNMT2 is suggested to be involved in the regulation of numerous processes, however its biological significance and underlying molecular mechanisms remain elusive. In the present study, we have used WI-38 and BJ human fibroblasts as an in vitro model system to investigate the effects of siRNA-based DNMT2 silencing. DNMT2-depleted cells were found to be sensitive to oxidative stress conditions as judged by increased production of reactive oxygen species and susceptible to DNA damage that resulted in the inhibition of cell proliferation. DNMT2 silencing promoted upregulation of proliferation-related and tumor suppressor miRNAs, namely miR-28-3p, miR-34a-3p, miR-30b-5p, miR-29b-3p, miR-200c-3p, miR-28-5p, miR-379-5p, miR-382-5p, miR-194-5p, miR-193b-3p and miR-409-3p. Moreover, DNMT2 silencing induced cellular senescence and DNMT2 levels were elevated in replicatively senescent cells. Taken together, we found that DNMT2 may take part in the regulation of cell proliferation and longevity in human fibroblasts and speculate that the manipulation of DNMT2 levels that limits cell proliferation may be potentially useful anticancer strategy.

Indexed as

Cell ProliferationDNA DamageOxidative StressApoptosisCell Cycle CheckpointsCell Line, TumorCellular SenescenceDNA (Cytosine-5-)-MethyltransferasesDNA MethylationFibroblastsHumansHydrogen PeroxideMicroRNAsReactive Oxygen SpeciesRNA InterferenceRNA, Small InterferingDNA (Cytosine-5-)-MethyltransferasesHydrogen PeroxideMicroRNAsReactive Oxygen SpeciesRNA, Small InterferingTRDMT1 protein, humanDNMT2FibroblastsGenotoxicitymiRNAsOxidative stressProliferation

Identifiers

PMID28843151
PMCPMC5568885
OpenAlexW2750174947

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.