Evidence map›Paper›PMID 30185144›Full record

ArticleBMC cancer2018

Increased insulin-like growth factor 1 production by polyploid adipose stem cells promotes growth of breast cancer cells.

Roberta Fajka-Boja, Annamária Marton, Anna Tóth, Péter Blazsó, Vilmos Tubak, Balázs Bálint, István Nagy, Zoltán Hegedűs, Csaba Vizler, Robert L Katona

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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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 1 institution in 1 country.

Roberta Fajka-BojaBiological Research Centre of the Hungarian Academy of Sciences, Institute of Genetics, H-6726 Temesvári krt. 62, Szeged, Hungary.
Annamária MartonBiological Research Centre of the Hungarian Academy of Sciences, Institute of Biochemistry, H-6726 Temesvári krt. 62, Szeged, Hungary.
Anna TóthBiological Research Centre of the Hungarian Academy of Sciences, Institute of Genetics, H-6726 Temesvári krt. 62, Szeged, Hungary.
Péter BlazsóBiological Research Centre of the Hungarian Academy of Sciences, Institute of Genetics, H-6726 Temesvári krt. 62, Szeged, Hungary.
Vilmos TubakCreative Laboratory Ltd, H-6726 Temesvári krt. 62, Szeged, Hungary.
Balázs BálintBiological Research Centre of the Hungarian Academy of Sciences, Institute of Biochemistry, H-6726 Temesvári krt. 62, Szeged, Hungary.
István NagyBiological Research Centre of the Hungarian Academy of Sciences, Institute of Biochemistry, H-6726 Temesvári krt. 62, Szeged, Hungary.
Zoltán HegedűsBiological Research Centre of the Hungarian Academy of Sciences, Institute of Biophysics, H-6726 Temesvári krt. 62, Szeged, Hungary.
Csaba VizlerBiological Research Centre of the Hungarian Academy of Sciences, Institute of Biochemistry, H-6726 Temesvári krt. 62, Szeged, Hungary.
Robert L KatonaBiological Research Centre of the Hungarian Academy of Sciences, Institute of Genetics, H-6726 Temesvári krt. 62, Szeged, Hungary. katona.robert@brc.mta.hu.ORCID http://orcid.org/0000-0002-7841-3118
HUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

National Research, Development and Innovation Office GINOP-2.3.2-15-2016-00001National Research, Development and Innovation Office GINOP-2.3.2-15-2016-00039
6 · The paper itself

Abstract

backgroundAdipose-tissue stem cells (ASCs) are subject of intensive research since their successful use in regenerative therapy. The drawback of ASCs is that they may serve as stroma for cancer cells and assist tumor progression. It is disquieting that ASCs frequently undergo genetic and epigenetic changes during their in vitro propagation. In this study, we describe the polyploidization of murine ASCs and the accompanying phenotypical, gene expressional and functional changes under long term culturing.

methodsASCs were isolated from visceral fat of C57BL/6 J mice, and cultured in vitro for prolonged time. The phenotypical changes were followed by microscopy and flow cytometry. Gene expressional changes were determined by differential transcriptome analysis and changes in protein expression were shown by Western blotting. The tumor growth promoting effect of ASCs was examined by co-culturing them with 4 T1 murine breast cancer cells.

resultsAfter five passages, the proliferation of ASCs decreases and cells enter a senescence-like state, from which a proportion of cells escape by polyploidization. The resulting ASC line is susceptible to adipogenic, osteogenic and chondrogenic differentiation, and expresses the stem cell markers CD29 and Sca-1 on an upregulated level. Differential transcriptome analysis of ASCs with normal and polyploid karyotype shows altered expression of genes that are involved in regulation of cancer, cellular growth and proliferation. We verified the increased expression of Klf4 and loss of Nestin on protein level. We found that elevated production of insulin-like growth factor 1 by polyploid ASCs rendered them more potent in tumor growth promotion in vitro.

conclusionsOur model indicates how ASCs with altered genetic background may support tumor progression.

Indexed as

PolyploidyAdipose TissueAnimalsAntigens, SurfaceBreast NeoplasmsCell Line, TumorCell ProliferationFemaleFlow CytometryGene Expression ProfilingHumansInsulin-Like Growth Factor IKaryotypeKruppel-Like Factor 4MiceStem CellsAntigens, SurfaceIGF1 protein, humanInsulin-Like Growth Factor IKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Adipose stem cellsBreast cancerInsulin-like growth factor 1PolyploidyTranscriptome

Identifiers

PMID30185144
PMCPMC6126028
OpenAlexW2892306827

What OpenQuestion holds

Textmetadata
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.