Evidence map›Paper›PMID 33727591›Full record

ArticleScientific reports2021

CD73 facilitates EMT progression and promotes lung metastases in triple-negative breast cancer.

Nataliia Petruk, Sanni Tuominen, Malin Åkerfelt, Jesse Mattsson, Jouko Sandholm, Matthias Nees, Gennady G Yegutkin, Arja Jukkola, Johanna Tuomela, Katri S Selander

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 74 citations in OpenAlex.

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  12. Adenosine Kinase: An Epigenetic Modulator and Drug Target.Journal of inherited metabolic disease · 2025
    Review
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  20. The Role of Adenosine in Overcoming Resistance in Sarcomas.International journal of molecular sciences · 2024
    Review
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 6 institutions in 2 countries.

Nataliia PetrukInstitute of Biomedicine, University of Turku, Turku, Finland.
Sanni TuominenInstitute of Biomedicine, University of Turku, Turku, Finland.
Malin ÅkerfeltInstitute of Biomedicine, University of Turku, Turku, Finland.
Jesse MattssonInstitute of Biomedicine, University of Turku, Turku, Finland.
Jouko SandholmTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Matthias NeesInstitute of Biomedicine, University of Turku, Turku, Finland.
Gennady G YegutkinMediCity Research Laboratory, University of Turku, Turku, Finland.
Arja JukkolaDepartment of Oncology, Tampere University Hospital, Tays Cancer Center, Tampere, Finland.
Johanna TuomelaInstitute of Biomedicine, University of Turku, Turku, Finland.
Katri S SelanderDepartment of Oncology, Oulu University Hospital, Oulu, Finland. Katri.Selander@ppshp.fi.
University of Turku · FIÅbo Akademi University · FIMedical University of Lublin · PLOulu University Hospital · FITampere University Hospital · FITurku Centre for Computer Science · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD73 is a cell surface ecto-5'-nucleotidase, which converts extracellular adenosine monophosphate to adenosine. High tumor CD73 expression is associated with poor outcome among triple-negative breast cancer (TNBC) patients. Here we investigated the mechanisms by which CD73 might contribute to TNBC progression. This was done by inhibiting CD73 with adenosine 5'-(α, β-methylene) diphosphate (APCP) in MDA-MB-231 or 4T1 TNBC cells or through shRNA-silencing (sh-CD73). Effects of such inhibition on cell behavior was then studied in normoxia and hypoxia in vitro and in an orthotopic mouse model in vivo. CD73 inhibition, through shRNA or APCP significantly decreased cellular viability and migration in normoxia. Inhibition of CD73 also resulted in suppression of hypoxia-induced increase in viability and prevented cell protrusion elongation in both normoxia and hypoxia in cancer cells. Sh-CD73 4T1 cells formed significantly smaller and less invasive 3D organoids in vitro, and significantly smaller orthotopic tumors and less lung metastases than control shRNA cells in vivo. CD73 suppression increased E-cadherin and decreased vimentin expression in vitro and in vivo, proposing maintenance of a more epithelial phenotype. In conclusion, our results suggest that CD73 may promote early steps of tumor progression, possibly through facilitating epithelial-mesenchymal transition.

Indexed as

Epithelial-Mesenchymal Transition5'-NucleotidaseAnimalsCell Line, TumorFemaleGPI-Linked ProteinsHumansLung NeoplasmsMammary Neoplasms, AnimalMiceMice, Inbred BALB CNeoplasm MetastasisNeoplasm ProteinsTriple Negative Breast Neoplasms5'-NucleotidaseGPI-Linked ProteinsNeoplasm ProteinsNT5E protein, human

Identifiers

PMID33727591
PMCPMC7966763
OpenAlexW3137737413

What OpenQuestion holds

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LicenceCC BY
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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.