Evidence map›Paper›PMID 26498687›Full record

ArticleOncotarget2015

Myeloma cells can corrupt senescent mesenchymal stromal cells and impair their anti-tumor activity.

Servet Özcan, Nicola Alessio, Mustafa Burak Acar, Güler Toprak, Zeynep Burcin Gönen, Gianfranco Peluso, Umberto Galderisi

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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  9. The Relationship Between Mesenchymal Stem Cells and Tumor Dormancy.Frontiers in cell and developmental biology · 2021
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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 4 institutions in 3 countries.

Servet ÖzcanGenome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey.
Nicola AlessioDepartment of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Naples, Italy.
Mustafa Burak AcarGenome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey.
Güler ToprakGenome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey.
Zeynep Burcin GönenGenome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey.
Gianfranco PelusoInstitute of Bioscience and Bioresources, CNR, Naples, Italy.
Umberto GalderisiGenome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Turkey.
Erciyes University · TRInstitute of Biosciences and Bioresources · ITUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescent cells secrete several molecules that help to prevent the progression of cancer. However, cancer cells can also misuse these secreted elements to survive and grow. Since the molecular and functional bases of these different elements remain poorly understood, we analyzed the effect of senescent mesenchymal stromal cell (MSC) secretome on the biology of ARH-77 myeloma cells. In addition to differentiating in mesodermal derivatives, MSCs have sustained interest among researchers by supporting hematopoiesis, contributing to tissue homeostasis, and modulating inflammatory response, all activities accomplished primarily by the secretion of cytokines and growth factors. Moreover, senescence profoundly affects the composition of MSC secretome. In this study, we induced MSC senescence by oxidative stress, DNA damage, and replicative exhaustion. While the first two are considered to induce acute senescence, extensive proliferation triggers replicative (i.e., chronic) senescence. We cultivated cancer cells in the presence of acute and chronic senescent MSC-conditioned media and evaluated their proliferation, DNA damage, apoptosis, and senescence. Our findings revealed that senescent secretomes induced apoptosis or senescence, if not both, to different extents. This anti-tumor activity became heavily impaired when secretomes were collected from senescent cells previously in contact (i.e., primed) with cancer cells. Our analysis of senescent MSC secretomes with LC-MS/MS followed by Gene Ontology classification further indicated that priming with cancer profoundly affected secretome composition by abrogating the production of pro-senescent and apoptotic factors. We thus showed for the first time that compared with cancer-primed MSCs, naïve senescent MSCs can exert different effects on tumor progression.

Indexed as

Cellular SenescenceAntineoplastic AgentsApoptosisAutophagyCell Line, TumorCell ProliferationCells, CulturedChromatography, LiquidCoculture TechniquesCulture Media, ConditionedDNA DamageHumansMesenchymal Stem CellsMultiple MyelomaTandem Mass SpectrometryAntineoplastic AgentsCulture Media, ConditionedapoptosiscancerGerotargetmesenchymal stem cellssecretomesenescence

Identifiers

PMID26498687
PMCPMC4741840
OpenAlexW1860229204

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.