Evidence map›Paper›PMID 23562655›Full record

ArticleExperimental cell research2013

Protein kinase D2 regulates migration and invasion of U87MG glioblastoma cells in vitro.

Eva Bernhart, Sabine Damm, Andrea Wintersperger, Trevor DeVaney, Andreas Zimmer, Tony Raynham, Christopher Ireson, Wolfgang Sattler

Open access · hybridAbstract read
In one paragraph

Article in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024
    Review
  8. Article
  9. Potential role for protein kinase D inhibitors in prostate cancer.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
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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 3 institutions in 2 countries.

Eva BernhartInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Sabine DammInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Andrea WinterspergerInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Trevor DeVaneyInstitute of Biophysics, Medical University of Graz, Austria.
Andreas ZimmerInstitute of Pharmaceutical Sciences, Department of Pharmaceutical Technology, Karl-Franzens University, Graz, Austria.
Tony RaynhamCancer Research Technology Ltd, London, UK.
Christopher IresonCancer Research Technology Ltd, London, UK.
Wolfgang SattlerInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria. Electronic address: wolfgang.sattler@medunigraz.at.
Medical University of Graz · ATCancer Research UK Technology · GBUniversity of Graz · AT

Funding

Austrian Science Fund FWF F 3007
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common malignant brain tumor, which, despite combined modality treatment, reoccurs and is invariably fatal for affected patients. Recently, a member of the serine/threonine protein kinase D (PRKD) family, PRKD2, was shown to be a potent mediator of glioblastoma growth. Here we studied the role of PRKD2 in U87MG glioblastoma cell migration and invasion in response to sphingosine-1-phosphate (S1P), an activator of PRKD2 and a GBM mitogen. Time-lapse microscopy demonstrated that random cell migration was significantly diminished in response to PRKD2 silencing. The pharmacological PRKD family inhibitor CRT0066101 decreased chemotactic migration and invasion across uncoated or matrigel-coated Transwell inserts. Silencing of PRKD2 attenuated migration and invasion of U87MG cells even more effectively. In terms of downstream signaling, CRT0066101 prevented PRKD2 autophosphorylation and inhibited p44/42 MAPK and to a smaller extent p54/46 JNK and p38 MAPK activation. PRKD2 silencing impaired activation of p44/42 MAPK and p54/46 JNK, downregulated nuclear c-Jun protein levels and decreased c-Jun(S73) phosphorylation without affecting the NFκB pathway. Finally, qPCR array analyses revealed that silencing of PRKD2 downregulates mRNA levels of integrin alpha-2 and -4 (ITGA2 and -4), plasminogen activator urokinase (PLAU), plasminogen activator urokinase receptor (PLAUR), and matrix metallopeptidase 1 (MMP1). Findings of the present study identify PRKD2 as a potential target to interfere with glioblastoma cell migration and invasion, two major determinants contributing to recurrence of glioblastoma after multimodality treatment.

Indexed as

Brain NeoplasmsCell Line, TumorCell MovementDrug Evaluation, PreclinicalGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGlioblastomaHumansLysophospholipidsMAP Kinase Signaling SystemNeoplasm InvasivenessProtein Kinase D2Protein Kinase InhibitorsProtein KinasesPyrimidinesRNA InterferenceCRT 0066101LysophospholipidsProtein Kinase D2Protein Kinase InhibitorsProtein KinasesPyrimidinesRNA, Small InterferingSphingosinesphingosine 1-phosphateC-JunGlioblastomaInvasionMAPKPRKD2Sphingosine-1-phosphate

Identifiers

PMID23562655
PMCPMC3715702
OpenAlexW2068482010

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.