Evidence map›Paper›PMID 26741507›Full record

ArticleOncotarget2016

Control of glioma cell migration and invasiveness by GDF-15.

Paula Codó, Michael Weller, Kerstin Kaulich, Daniel Schraivogel, Manuela Silginer, Guido Reifenberger, Gunter Meister, Patrick Roth

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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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 5 institutions in 2 countries.

Paula CodóLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
Michael WellerLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
Kerstin KaulichDepartment of Neuropathology, Heinrich Heine University, Düsseldorf, and German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Daniel SchraivogelDepartment of Biochemistry I, University of Regensburg, Regensburg, Germany.
Manuela SilginerLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
Guido ReifenbergerDepartment of Neuropathology, Heinrich Heine University, Düsseldorf, and German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Gunter MeisterDepartment of Biochemistry I, University of Regensburg, Regensburg, Germany.
Patrick RothLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
University Hospital of Zurich · CHUniversity of Regensburg · DEGerman Cancer Research Center · DEHeidelberg University · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth and differentiation factor (GDF)-15 is a member of the transforming growth factor (TGF)-β family of proteins. GDF-15 levels are increased in the blood and cerebrospinal fluid of glioblastoma patients. Using a TCGA database interrogation, we demonstrate that high GDF-15 expression levels are associated with poor survival of glioblastoma patients. To elucidate the role of GDF-15 in glioblastoma in detail, we confirmed that glioma cells express GDF-15 mRNA and protein in vitro. To allow for a detailed functional characterization, GDF-15 expression was silenced using RNA interference in LNT-229 and LN-308 glioma cells. Depletion of GDF-15 had no effect on cell viability. In contrast, GDF-15-deficient cells displayed reduced migration and invasion, in the absence of changes in Smad2 or Smad1/5/8 phosphorylation. Conversely, exogenous GDF-15 stimulated migration and invasiveness. Large-scale expression profiling revealed that GDF-15 gene silencing resulted in minor changes in the miRNA profile whereas several genes, including members of the plasminogen activator/inhibitor complex, were deregulated at the mRNA level. One of the newly identified genes induced by GDF-15 gene silencing was the serpin peptidase inhibitor, clade E nexin group 1 (serpine1) which is induced by TGF-β and known to inhibit migration and invasiveness. However, serpine1 down-regulation alone did not mediate GDF-15-induced promotion of migration and invasiveness. Our findings highlight the complex contributions of GDF-15 to the invasive phenotype of glioma cells and suggest anti-GDF-15 approaches as a promising therapeutic strategy.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticApoptosisBlotting, WesternBrain NeoplasmsCell ProliferationGene Expression ProfilingGliomaGrowth Differentiation Factor 15HumansImmunoenzyme TechniquesMicroRNAsNeoplasm InvasivenessNeoplasm StagingPrognosisReal-Time Polymerase Chain ReactionGDF15 protein, humanGrowth Differentiation Factor 15MicroRNAsRNA, MessengerGDF-15glioblastomainvasionserpine1TCGA

Identifiers

PMID26741507
PMCPMC4884950
OpenAlexW2267640958

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.