Evidence map›Paper›PMID 29259202›Full record

ArticleScientific reports2017

Identification of new genes associated to senescent and tumorigenic phenotypes in mesenchymal stem cells.

Joana Cristina Medeiros Tavares Marques, Déborah Afonso Cornélio, Vivian Nogueira Silbiger, André Ducati Luchessi, Sandro de Souza, Silvia Regina Batistuzzo de Medeiros

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

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  18. NADCommunications biology · 2020
    Article
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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

6 authors.

Joana Cristina Medeiros Tavares MarquesFaculdade de Ciências da Saúde do Trairi (FACISA), Universidade Federal do Rio Grande do Norte (UFRN), Rua Traíri, S/N, Centro, Santa Cruz, Rio Grande do Norte (RN), 59200-000, Brazil.
Déborah Afonso CornélioLaboratório de Biologia Molecular e Genômica, Centro de Biociências, UFRN, Campus Universitário, Avenida Senador Salgado Filho, 3000, Lagoa nova, Natal, RN, 59078-900, Brazil.
Vivian Nogueira SilbigerDepartamento de Análises Clínicas e Toxicológicas, Centro de Ciências da Saúde, CCS/UFRN, Av General Cordeiro de Farias S/N, Petropolis, Natal, 59010-115, RN, Brazil.
André Ducati LuchessiDepartamento de Análises Clínicas e Toxicológicas, Centro de Ciências da Saúde, CCS/UFRN, Av General Cordeiro de Farias S/N, Petropolis, Natal, 59010-115, RN, Brazil.
Sandro de SouzaInstituto do Cérebro, Instituto de Metrópole Digital, UFRN, Av. Nascimento de Castro, 2155, UFRN, 59056-450, RN, Brazil.
Silvia Regina Batistuzzo de MedeirosLaboratório de Biologia Molecular e Genômica, Centro de Biociências, UFRN, Campus Universitário, Avenida Senador Salgado Filho, 3000, Lagoa nova, Natal, RN, 59078-900, Brazil. sbatistu@cb.ufrn.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although human mesenchymal stem cells (hMSCs) are a powerful tool for cell therapy, prolonged culture times result in replicative senescence or acquisition of tumorigenic features. To identify a molecular signature for senescence, we compared the transcriptome of senescent and young hMSCs with normal karyotype (hMSCs/n) and with a constitutional inversion of chromosome 3 (hMSC/inv). Senescent and young cells from both lineages showed differentially expressed genes (DEGs), with higher levels in senescent hMSCs/inv. Among the 30 DEGs in senescent hMSC/inv, 11 are new candidates for biomarkers of cellular senescence. The functional categories most represented in senescent hMSCs were related to cellular development, cell growth/proliferation, cell death, cell signaling/interaction, and cell movement. Mapping of DEGs onto biological networks revealed matrix metalloproteinase-1, thrombospondin 1, and epidermal growth factor acting as topological bottlenecks. In the comparison between senescent hMSCs/n and senescent hMSCs/inv, other functional annotations such as segregation of chromosomes, mitotic spindle formation, and mitosis and proliferation of tumor lines were most represented. We found that many genes categorized into functional annotations related to tumors in both comparisons, with relation to tumors being highest in senescent hMSCs/inv. The data presented here improves our understanding of the molecular mechanisms underlying the onset of cellular senescence as well as tumorigenesis.

Indexed as

BiomarkersCarcinogenesisCell DeathCell MovementCell ProliferationCells, CulturedCellular SenescenceChromosome SegregationChromosomes, Human, Pair 3HumansMesenchymal Stem CellsMitosisMolecular Sequence AnnotationPhenotypeSignal TransductionBiomarkers

Identifiers

PMID29259202
PMCPMC5736717

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Registered trials

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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.