Evidence map›Paper›PMID 33187081›Full record

ArticlePharmaceuticals (Basel, Switzerland)2020

Enzymatic Activity of CD73 Modulates Invasion of Gliomas via Epithelial-Mesenchymal Transition-Like Reprogramming.

Julia Tsiampali, Silke Neumann, Beatriz Giesen, Katharina Koch, Donata Maciaczyk, Christoph Janiak, Daniel Hänggi, Jaroslaw Maciaczyk

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  6. CD73 promotes non-small cell lung cancer metastasis by regulating Axl signaling independent of GAS6.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

8 authors at 4 institutions in 2 countries.

Julia TsiampaliNeurosurgery Department, University Hospital Duesseldorf, 40225 Duesseldorf, Germany.ORCID 0000-0002-2880-5703
Silke NeumannDepartment of Pathology, University of Otago, Dunedin 9016, New Zealand.
Beatriz GiesenInstitute of Inorganic Chemistry and Structural Chemistry, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.
Katharina KochNeurosurgery Department, University Hospital Duesseldorf, 40225 Duesseldorf, Germany.
Donata MaciaczykDepartment of Pathology, University of Otago, Dunedin 9016, New Zealand.
Christoph JaniakInstitute of Inorganic Chemistry and Structural Chemistry, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.ORCID 0000-0002-6288-9605
Daniel HänggiNeurosurgery Department, University Hospital Duesseldorf, 40225 Duesseldorf, Germany.
Jaroslaw MaciaczykDepartment of Neurosurgery, University Hospital Bonn, 53179 Bonn, Germany.
Düsseldorf University Hospital · DEHeinrich Heine University Düsseldorf · DEUniversity of Otago · NZUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive malignant primary brain tumour in adulthood. Despite strong research efforts current treatment options have a limited impact on glioma stem-like cells (GSCs) which contribute to GBM formation, progression and chemoresistance. Invasive growth of GSCs is in part associated with epithelial-mesenchymal-like transition (EMT), a mechanism associated with CD73 in several cancers. Here, we show that CD73 regulates the EMT activator SNAIL1 and further investigate the role of enzymatic and non-enzymatic CD73 activity in GBM progression. Reduction of CD73 protein resulted in significant suppression of GSC viability, proliferation and clonogenicity, whereas CD73 enzymatic activity exhibited negative effects only on GSC invasion involving impaired downstream adenosine (ADO) signalling. Furthermore, application of phosphodiesterase inhibitor pentoxifylline, a potent immunomodulator, effectively inhibited ZEB1 and CD73 expression and significantly decreased viability, clonogenicity, and invasion of GSC in vitro cultures. Given the involvement of adenosine and A

Indexed as

A3ARadenosineCD73drug targetsepithelial–mesenchymal transitionglioblastoma

Identifiers

PMID33187081
PMCPMC7698190
OpenAlexW3105116134

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.