Evidence map›Paper›PMID 32707902›Full record

ArticleCells2020

Fibroblast Growth Factor-14 Acts as Tumor Suppressor in Lung Adenocarcinomas.

Kati Turkowski, Frederik Herzberg, Stefan Günther, David Brunn, Andreas Weigert, Michael Meister, Thomas Muley, Mark Kriegsmann, Marc A Schneider, Hauke Winter and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 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
1.1field-weighted citation impact, top 24% 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, 27 citations in OpenAlex.

  1. Review
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  11. Long non-coding RNAPeerJ · 2022
    Article
  12. Review
  13. Collagen XI alpha 1 chain, a potential therapeutic target for cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Review
  14. Review
  15. 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

15 authors at 4 institutions in 1 country.

Kati TurkowskiMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Frederik HerzbergMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Stefan GüntherMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
David BrunnMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, 60590 Frankfurt, Germany.ORCID 0000-0002-7529-1952
Michael MeisterTranslational Research Unit, Thoraxklinik at Heidelberg University, 69126 Heidelberg, Germany.
Thomas MuleyTranslational Research Unit, Thoraxklinik at Heidelberg University, 69126 Heidelberg, Germany.
Mark KriegsmannTranslational Lung Research Center (TLRC) Heidelberg, 69126 Heidelberg, Germany.ORCID 0000-0002-7319-3646
Marc A SchneiderTranslational Research Unit, Thoraxklinik at Heidelberg University, 69126 Heidelberg, Germany.ORCID 0000-0001-8269-3821
Hauke WinterTranslational Lung Research Center (TLRC) Heidelberg, 69126 Heidelberg, Germany.
Michael ThomasTranslational Lung Research Center (TLRC) Heidelberg, 69126 Heidelberg, Germany.
Friedrich GrimmingerDepartment of Internal Medicine, Justus Liebig University, 35392 Giessen, Germany.
Werner SeegerMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Soni Savai PullamsettiMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Rajkumar SavaiMax Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.ORCID 0000-0003-1538-2091
Heidelberg University · DEMax Planck Institute for Heart and Lung Research · DEJustus-Liebig-Universität Gießen · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Investigation of the molecular dynamics in lung cancer is crucial for the development of new treatment strategies. Fibroblast growth factor (FGF) 14 belongs to the FGF family, which might play a crucial role in cancer progression. We analyzed lung adenocarcinoma (LUAC) patients samples and found that FGF14 was downregulated, correlating with reduced survival and oncogenic mutation status. FGF14 overexpression in lung cancer cell lines resulted in decreased proliferation, colony formation, and migration, as well as increased expression of epithelial markers and a decreased expression of mesenchymal markers, indicating a mesenchymal to epithelial transition in vitro. We verified these findings using small interfering RNA against FGF14 and further confirmed the suppressive effect of FGF14 in a

Indexed as

A549 CellsAdenocarcinoma of LungAnimalsCell MovementCell ProliferationCohort StudiesDown-RegulationEpithelial-Mesenchymal TransitionFibroblast Growth FactorsHumansKaplan-Meier EstimateLung NeoplasmsMiceMice, Inbred NODMice, SCIDTranscriptomefibroblast growth factor 14Fibroblast Growth FactorsTumor Suppressor Proteinsfibroblast growth factor 14lung adenocarcinomalung cancer mesenchymal epithelial transitionxenograft model

Identifiers

PMID32707902
PMCPMC7466013
OpenAlexW3044501928

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.