Evidence map›Paper›PMID 25682201›Full record

ArticleOncotarget2015

RasGRP3 regulates the migration of glioma cells via interaction with Arp3.

Hae Kyung Lee, Susan Finniss, Simona Cazacu, Cunli Xiang, Laila M Poisson, Peter M Blumberg, Chaya Brodie

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. Article
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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

7 authors at 2 institutions in 2 countries.

Hae Kyung LeeDavidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Susan FinnissDavidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Simona CazacuDavidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Cunli XiangDavidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Laila M PoissonHermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Peter M BlumbergLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Chaya BrodieDavidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA.
Henry Ford Hospital · USNational Cancer Institute · US

Funding

Molecular Mechanism of Action of Phorbol EsterZIABC005270 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BLUMBERG, PETER · 2009 to 2018
$18.4M
Regulation of Glioma Cell Migration by RasGRP3R01NS066303 · NINDS · HENRY FORD HEALTH SYSTEM · PI BRODIE, CHAYA · 2009 to 2010
$733k
Intramural NIH HHS ZIA BC005270NINDS NIH HHS 01-NS066303NINDS NIH HHS R01 NS066303
6 · The paper itself

Abstract

Glioblastoma (GBM), the most aggressive primary brain tumors, are highly infiltrative. Although GBM express high Ras activity and Ras proteins have been implicated in gliomagenesis, Ras-activating mutations are not frequent in these tumors. RasGRP3, an important signaling protein responsive to diacylglycerol (DAG), increases Ras activation. Here, we examined the expression and functions of RasGRP3 in GBM and glioma cells. RasGRP3 expression was upregulated in GBM specimens and glioma stem cells compared with normal brains and neural stem cells, respectively. RasGRP3 activated Ras and Rap1 in glioma cells and increased cell migration and invasion partially via Ras activation. Using pull-down assay and mass spectroscopy we identified the actin-related protein, Arp3, as a novel interacting protein of RasGRP3. The interaction of RasGRP3 and Arp3 was validated by immunofluorescence staining and co-immunoprecipitation, and PMA, which activates RasGRP3 and induces its translocation to the peri-nuclear region, increased the association of Arp3 and RasGRP3. Arp3 was upregulated in GBM, regulated cell spreading and migration and its silencing partially decreased these effects of RasGRP3 in glioma cells. In summary, RasGRP3 acts as an important integrating signaling protein of the DAG and Ras signaling pathways and actin polymerization and represents an important therapeutic target in GBM.

Indexed as

Actin-Related Protein 3Brain NeoplasmsCell Line, TumorCell MovementGliomaGuanine Nucleotide Exchange FactorsHumansras Guanine Nucleotide Exchange FactorsSignal TransductionTransfectionActin-Related Protein 3ACTR3 protein, humanGuanine Nucleotide Exchange FactorsRASGRP3 protein, humanras Guanine Nucleotide Exchange Factors

Identifiers

PMID25682201
PMCPMC4359336
OpenAlexW1593801960

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.