Evidence map›Paper›PMID 32378800›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2020

Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.

Jakob Paur, Maximilian Valler, Rebecca Sienel, Karin Taxauer, Klaus Holzmann, Brigitte Marian, Andreas Unterberger, Thomas Mohr, Walter Berger, Andja Gvozdenovich and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  5. FGF9 Recruits β-Catenin to Increase Hepatic ECM Synthesis and Promote NASH-Driven HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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  13. Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2020
    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

13 authors at 1 institution in 1 country.

Jakob PaurDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Maximilian VallerDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Rebecca SienelDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Karin TaxauerDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Klaus HolzmannDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Brigitte MarianDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0001-7034-5563
Andreas UnterbergerDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Thomas MohrDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0002-1933-847X
Walter BergerDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0003-0014-1658
Andja GvozdenovichDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Johannes SchimmingDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Michael GruschDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0001-5486-9340
Bettina Grasl-KrauppDepartment of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0003-4889-6531
Comprehensive Cancer Center Vienna · AT

Funding

Austrian Science Fund FWF P 30105
6 · The paper itself

Abstract

BACKGROUND &

aimsRecently, overexpression of the fibroblast growth factor receptor 3 (FGFR3) splice variants FGFR3-IIIb and FGFR3-IIIc was found in ~50% of hepatocellular carcinoma (HCC). Here, we aim to identify FGFR3-IIIb/IIIc ligands, which drive the progression of HCC.

methodsFACS, MTT assay and/or growth curves served to identify the FGFR3-IIIb/IIIc ligand being most effective to induce growth of hepatoma/hepatocarcinoma cell lines, established from human HCC. The most potent FGF was characterized regarding the expression levels in epithelial and stromal cells of liver and HCC and impact on neoangiogenesis, clonogenicity and invasive growth of hepatoma/hepatocarcinoma cells.

resultsAmong all FGFR3-IIIb/IIIc ligands tested, FGF9 was the most potent growth factor for hepatoma/hepatocarcinoma cells. Replication and/or sprouting of blood/lymphendothelial cells was stimulated as well. FGF9 occurred mainly in stromal cells of unaltered liver but in epithelial cells of HCC. Every fifth HCC exhibited overexpressed FGF9 and frequent co-upregulation of FGFR3-IIIb/IIIc. In hepatoma/hepatocarcinoma cells FGF9 enhanced the capability for clonogenicity and disintegration of the blood and lymphatic endothelium, being most pronounced in cells overexpressing FGFR3-IIIb or FGFR3-IIIc, respectively. Any of the FGF9 effects in hepatoma/hepatocarcinoma cells was blocked completely by applying the FGFR1-3-specific tyrosine kinase inhibitor BGJ398 or siFGFR3, while siFGFR1/2/4 were mostly ineffective.

conclusionsFGF9 acts via FGFR3-IIIb/IIIc to enhance growth and aggressiveness of HCC cells. Accordingly, blockade of the FGF9-FGFR3-IIIb/IIIc axis may be an efficient therapeutic option for HCC patients.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsEpithelial CellsFibroblast Growth Factor 9HumansReceptor, Fibroblast Growth Factor, Type 3Up-RegulationFGF9 protein, humanFGFR3 protein, humanFibroblast Growth Factor 9Receptor, Fibroblast Growth Factor, Type 3fibroblast growth factor 9hepatocellular carcinomamalignant phenotypetumour progression

Identifiers

PMID32378800
PMCPMC7496895
OpenAlexW3023658761

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.