Evidence map›Paper›PMID 29030596›Full record

ArticleScientific reports2017

Mesenchymal stem cells from tumor microenvironment favour breast cancer stem cell proliferation, cancerogenic and metastatic potential, via ionotropic purinergic signalling.

A Maffey, C Storini, C Diceglie, C Martelli, L Sironi, C Calzarossa, N Tonna, R Lovchik, E Delamarche, L Ottobrini and 1 more

Open access · goldAbstract 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 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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  16. Mesenchymal stem/stromal cells in cancer therapy.Journal of hematology & oncology · 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

11 authors at 4 institutions in 2 countries.

A MaffeyNeuro-Zone srl, OpenZone Via Ariosto 21, 20091, Bresso (MI), Italy.
C StoriniSanipedia srl, OpenZone Via Ariosto 21, 20091, Bresso (MI), Italy.
C DiceglieDepartment of Pathophysiology and Transplantation, University of Milan, Via F.lli Cervi 93, 20090, Segrate, Milano, Italy.
C MartelliDepartment of Pathophysiology and Transplantation, University of Milan, Via F.lli Cervi 93, 20090, Segrate, Milano, Italy.
L SironiSanipedia srl, OpenZone Via Ariosto 21, 20091, Bresso (MI), Italy.
C CalzarossaFondazione Fernando Santarelli, Neuroinflammation Lab, Corso Venezia 18, 20122, Milano, Italy.
N TonnaNeuro-Zone srl, OpenZone Via Ariosto 21, 20091, Bresso (MI), Italy.
R LovchikIBM Research, Zurich, Saeumerstrasse 4, 8803, Rueschlikon, Switzerland.
E DelamarcheIBM Research, Zurich, Saeumerstrasse 4, 8803, Rueschlikon, Switzerland.
L OttobriniDepartment of Pathophysiology and Transplantation, University of Milan, Via F.lli Cervi 93, 20090, Segrate, Milano, Italy.ORCID 0000-0002-5002-6845
F BiancoFondazione Fernando Santarelli, Neuroinflammation Lab, Corso Venezia 18, 20122, Milano, Italy. Fabio.bianco@fondazionesantarelli.org.
University of Milan · ITIBM Research - Zurich · CHNeuro-Zone (Italy) · ITPirelli (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interaction between tumor cells and the microenvironment is key in initiation, progression, and invasiveness of cancer. In particular, mesenchymal stem cells (MSCs) are recruited to the sites of developing tumors, thus promoting metastasis formation. Although it is well known that MSCs migrate and integrate in the tumor microenvironment (TME), their fate and function inside the tumor is still not clear. In this study, we analyzed the role played by MSCs in breast cancer oncogenesis. Data indicate that interaction of breast cancer cells with MSCs results in an increased proliferation and metabolic activity of breast cancer cells, partially due to MSC-derived microvesicles that are shed in the TME. Moreover, we addressed the question of whether we could modulate such interaction by acting on P2X-mediated intercellular communication. By inhibiting P2X-mediated purinergic signaling, we succeeded in reducing both the cancerogenic as well as the metastatic potential of breast cancer cells co-cultured with MSCs, in 2D as well as in 3D in vitro models. Data obtained demonstrate for the first time that the trophic effect of MSCs on breast cancer cell growth is exerted via ionotropic purinergic signaling, thus suggesting the inhibition of the purinergic signaling system as a potential target for therapeutic intervention.

Indexed as

Cell Line, TumorCell ProliferationCoculture TechniquesHumansMesenchymal Stem CellsNeoplastic Stem CellsReceptors, Purinergic P2XSignal TransductionTumor MicroenvironmentReceptors, Purinergic P2X

Identifiers

PMID29030596
PMCPMC5640614
OpenAlexW2760935141

What OpenQuestion holds

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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.