Evidence map›Paper›PMID 31374860›Full record

ArticleCells2019

Sprouty3 and Sprouty4, Two Members of a Family Known to Inhibit FGF-Mediated Signaling, Exert Opposing Roles on Proliferation and Migration of Glioblastoma-Derived Cells.

Burcu Emine Celik-Selvi, Astrid Stütz, Christoph-Erik Mayer, Jihen Salhi, Gerald Siegwart, Hedwig Sutterlüty

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Sprouty in Tumors of the Nervous System.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Role of SPRY4 in health and disease.Frontiers in oncology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. FGF2: a novel druggable target for glioblastoma?Expert opinion on therapeutic targets · 2020
    Review
  18. Article
  19. Article
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

6 authors at 1 institution in 1 country.

Burcu Emine Celik-SelviInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria.
Astrid StützInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria.
Christoph-Erik MayerInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria.
Jihen SalhiInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria.
Gerald SiegwartInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria.
Hedwig SutterlütyInstitute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center, Medical University of Vienna, A-1090 Vienna, Austria. hedwig.sutterluety@meduniwien.ac.at.ORCID 0000-0001-9249-9299
Comprehensive Cancer Center Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of receptor tyrosine kinase-induced pathways is a critical step driving the oncogenic potential of brain cancer. In this study, we investigated the role of two members of the Sprouty (Spry) family in brain cancer-derived cell lines. Using immunoblot analyses we found essential differences in the pattern of endogenous Spry3 and Spry4 expression. While Spry4 expression was mitogen-dependent and repressed in a number of cells from higher malignant brain cancers, Spry3 levels neither fluctuated in response to serum withdrawal nor were repressed in glioblastoma (GBM)-derived cell lines. In accordance to the well-known inhibitory role of Spry proteins in fibroblast growth factor (FGF)-mediated signaling, both Spry proteins were able to interfere with FGF-induced activation of the MAPK pathway although to a different extent. In response to serum solely, Spry4 exerts its role as a negative regulator of MAPK activation. Ectopic expression of Spry4 inhibited proliferation and migration of GBM-originated cells, positioning it as a tumor suppressor in brain cancer. In contrast, elevated Spry3 levels accelerated both proliferation and migration of these cell lines, while repression of Spry3 levels using shRNA caused a significant diminished growth and migration velocity rate of a GBM-derived cell line. This argues for a tumor-promoting function of Spry3 in GBMs. Based on these data we conclude that Spry3 and Spry4 fulfill different if not opposing roles within the cancerogenesis of brain malignancies.

Indexed as

Brain NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationGlioblastomaHumansIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsRNA, Small InterferingSignal TransductionIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsRNA, Small InterferingSPRY3 protein, humanSPRY4 protein, humanbrain cancerFGF-mediated signalingSprouty proteinstumor promotertumor suppressor

Identifiers

PMID31374860
PMCPMC6721513
OpenAlexW2964352679

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.