Evidence map›Paper›PMID 30567518›Full record

ArticleBMC cancer2018

ADSCs and adipocytes are the main producers in the autotaxin-lysophosphatidic acid axis of breast cancer and healthy mammary tissue in vitro.

Rafael Schmid, Katharina Wolf, Jan W Robering, Selina Strauß, Pamela L Strissel, Reiner Strick, Matthias Rübner, Peter A Fasching, Raymund E Horch, Andreas E Kremer and 2 more

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  8. The pleiotropic roles of adipocyte secretome in remodeling breast cancer.Journal of experimental & clinical cancer research : CR · 2022
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  16. Cancer-associated adipocytes: emerging supporters in breast cancer.Journal of experimental & clinical cancer research : CR · 2020
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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

12 authors at 1 institution in 1 country.

Rafael SchmidDepartment of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Krankenhausstr. 12, 91054, Erlangen, Germany.
Katharina WolfDepartment of Medicine I, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Jan W RoberingDepartment of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Krankenhausstr. 12, 91054, Erlangen, Germany.
Selina StraußDepartment of Medicine I, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Pamela L StrisselLaboratory for Molecular Medicine, Department of Gynecology and Obstetrics, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Reiner StrickLaboratory for Molecular Medicine, Department of Gynecology and Obstetrics, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Matthias RübnerLaboratory for Molecular Medicine, Department of Gynecology and Obstetrics, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Peter A FaschingDepartment of Gynecology and Obstetrics, Comprehensive Cancer Center Erlangen ER-EMN, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Raymund E HorchDepartment of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Krankenhausstr. 12, 91054, Erlangen, Germany.
Andreas E KremerDepartment of Medicine I, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Anja M BoosDepartment of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Krankenhausstr. 12, 91054, Erlangen, Germany.
Annika WeigandDepartment of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital of Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Krankenhausstr. 12, 91054, Erlangen, Germany. annika.weigand@uk-erlangen.de.ORCID http://orcid.org/0000-0003-0583-1412
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Deutsche Forschungsgemeinschaft KR4391/1-1ELAN-Fonds 13-12-11-1-WeigandInterdisziplinäres Zentrum für Klinische Forschung, Universitätsklinikum Erlangen E27
6 · The paper itself

Abstract

backgroundBreast cancer is the most common malignancy in women affecting one out of eight females throughout their lives. Autotaxin (ATX) is upregulated in breast cancer which results in increased lysophosphatidic acid (LPA) formation within the tumor. This study's aim was to identify the role of different mammary cell populations within the ATX-LPA axis.

methodsEpithelial-cell-adhesion-molecule-positive (EpCAM) and -negative cells from breast tumors, adipose-derived stem cells (ADSCs) of tumor-adjacent and tumor-distant mammary fat were isolated and compared to healthy ADSCs, mammary epithelial cells (HMECs), and mesenchymal cells (MES) of healthy mammary tissue (n = 4 each) and further to well-established breast (cancer) cell lines.

resultsmRNA expression analyses revealed that ADSCs and MES largely expressed LPA receptor 1 (LPAR1) while epithelial cells mainly expressed LPAR6. LPA 18:1 activated all the cell populations and cell lines by rise in cytosolic free calcium concentrations. MES and ADSCs expressed ATX whereas epithelial cells did not. ADSCs revealed the highest expression in ATX with a significant decline after adipogenic differentiation in healthy ADSCs, whereas ATX expression increased in ADSCs from tumor patients. Breast (cancer) cell lines did not express ATX. Transmigration of MES was stimulated by LPA whereas an inhibitory effect was observed in epithelial cells with no differences between tumors and healthy cells. Triple-negative breast cancer (TNBC) cell lines were also stimulated and the transmigration partly inhibited using the LPA receptor antagonist Ki16425.

conclusionsWe here show that each mammary cell population plays a different role in the ATX-LPA axis with ADSCs and adipocytes being the main source of ATX in tumor patients in our experimental setting. Inhibitors of this axis may therefore present a valuable target for pharmacological therapies.

Indexed as

AdipocytesCell DifferentiationCell LineageCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansLysophospholipase DLysophospholipidsMammary Glands, HumanMesenchymal Stem CellsPhosphoric Diester HydrolasesReceptors, Lysophosphatidic AcidRNA, MessengerTriple Negative Breast NeoplasmsLPAR1 protein, humanLPAR6 protein, humanlysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesReceptors, Lysophosphatidic AcidRNA, MessengerADSCAutotaxinBreast cancerLysophosphatidic acidTherapy

Identifiers

PMID30567518
PMCPMC6300006
OpenAlexW2904770274

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.