Evidence map›Paper›PMID 22966858›Full record

ArticleMolecular cancer2012

The small GTPase RhoG mediates glioblastoma cell invasion.

Aneta Kwiatkowska, Sebastien Didier, Shannon Fortin, Yayu Chuang, Timothy White, Michael E Berens, Elisabeth Rushing, Jennifer Eschbacher, Nhan L Tran, Amanda Chan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  12. RhoG-Rac1 Signaling Pathway Mediates Metabolic Dysfunction of the Pancreatic Beta-Cells Under Chronic Hyperglycemic Conditions.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Article
  13. Article
  14. Article
  15. The Role of Rho GTPases in Motility and Invasion of Glioblastoma Cells.Analytical cellular pathology (Amsterdam) · 2020
    Review
  16. Review
  17. The Role of Rho GTPases in VEGF Signaling in Cancer Cells.Analytical cellular pathology (Amsterdam) · 2020
    Review
  18. 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

11 authors at 4 institutions in 2 countries.

Aneta KwiatkowskaCenter for Oncology and Cell Biology, The Feinstein Institute for Medical Research at North Shore-LIJ, Manhasset, NY, USA.
Sebastien Didier
Shannon Fortin
Yayu Chuang
Timothy White
Michael E Berens
Elisabeth Rushing
Jennifer Eschbacher
Nhan L Tran
Amanda Chan
Marc Symons
Feinstein Institute for Medical Research · USTranslational Genomics Research Institute · USBarrow Neurological Institute · USUniversity Hospital of Zurich · CH

Funding

Targeting the Fn14-Rac1 signaling pathway in invasive gliomasR01CA130940 · NCI · TRANSLATIONAL GENOMICS RESEARCH INST · PI TRAN, NHAN L · 2008 to 2012
$1.5M
Identification of RhoGEFs as novel therapeutic targets for malignant gliomaR21NS060023 · NINDS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SYMONS, MARC H · 2007 to 2008
$400k
NCI NIH HHS R01 CA130940NINDS NIH HHS NS060023
6 · The paper itself

Abstract

backgroundThe invasion of glioblastoma cells into regions of the normal brain is a critical factor that limits current therapies for malignant astrocytomas. Previous work has identified roles for the Rho family guanine nucleotide exchange factors Trio and Vav3 in glioblastoma invasion. Both Trio and Vav3 act on the small GTPase RhoG. We therefore examined the role of RhoG in the invasive behavior of glioblastoma cells.

resultsWe found that siRNA-mediated depletion of RhoG strongly inhibits invasion of glioblastoma cells through brain slices ex vivo. In addition, depletion of RhoG has a marginal effect on glioblastoma cell proliferation, but significantly inhibits glioblastoma cell survival in colony formation assays. We also observed that RhoG is activated by both HGF and EGF, two factors that are thought to be clinically relevant drivers of glioblastoma invasive behavior, and that RhoG is overexpressed in human glioblastoma tumors versus non-neoplastic brain. In search of a mechanism for the contribution of RhoG to the malignant behavior of glioblastoma cells, we found that depletion of RhoG strongly inhibits activation of the Rac1 GTPase by both HGF and EGF. In line with this observation, we also show that RhoG contributes to the formation of lamellipodia and invadopodia, two functions that have been shown to be Rac1-dependent.

conclusionsOur functional analysis of RhoG in the context of glioblastoma revealed a critical role for RhoG in tumor cell invasion and survival. These results suggest that targeting RhoG-mediated signaling presents a novel avenue for glioblastoma therapy.

Indexed as

AnimalsBrain NeoplasmsCell Growth ProcessesEpidermal Growth FactorErbB ReceptorsGlioblastomaHumansMiceNeoplasm InvasivenessNeuropeptidesPseudopodiaPutamenrac1 GTP-Binding Proteinrac GTP-Binding Proteinsrho GTP-Binding ProteinsRNA, Small InterferingEpidermal Growth FactorErbB ReceptorsNeuropeptidesrac1 GTP-Binding ProteinRac1 protein, mouserac GTP-Binding Proteinsrho GTP-Binding ProteinsRNA, Small Interfering

Identifiers

PMID22966858
PMCPMC3557187
OpenAlexW2125492661

What OpenQuestion holds

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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.