ArticleOncotarget2016
A role for activated Cdc42 in glioblastoma multiforme invasion.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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.
Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Systems biology-driven drug repurposing in glioblastomaResearch in pharmaceutical sciences · 2026Article
- The impact of inhibiting the Hippo signaling pathway effector molecule YAP1 on in vitro glioblastoma and glioblastoma stem cells.Scientific reports · 2026Article
- Proapoptotic and antimigration properties of osthole in combination with LY294002 against human glioma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- IQ motif family genes in male infertility: pathogenesis, mechanisms, and clinical perspectives.Frontiers in reproductive health · 2025Review
- IQGAP1: cross-disease target via receptor-pathway networks.Frontiers in oncology · 2025Review
- Bioinformatics Examination of Glioblastoma Identifies a Potential Panel of Therapeutic Biomarkers.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Role of scaffold proteins in the heterogeneity of glioblastoma.Cell communication and signaling : CCS · 2024Review
- Differences and similarities in biophysical and biological characteristics between U87 MG glioblastoma and astrocyte cells.Histochemistry and cell biology · 2024Article
- Design and Computational Analysis of an MMP9 Inhibitor in Hypoxia-Induced Glioblastoma Multiforme.ACS omega · 2023Article
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- miR-218 affects the ECM composition and cell biomechanical properties of glioblastoma cells.Journal of cellular and molecular medicine · 2022Article
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- Article
- Novel CTRP8-RXFP1-JAK3-STAT3 axis promotes Cdc42-dependent actin remodeling for enhanced filopodia formation and motility in human glioblastoma cells.Molecular oncology · 2022Article
- AmotL2, IQGAP1, and FKBP51 Scaffold Proteins in Glioblastoma Stem Cell Niches.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Review
- Analysis of Circulating miRNA Profile in Plasma Samples of Glioblastoma Patients.International journal of molecular sciences · 2021Article
- The roles of Cdc42 and Rac1 in the formation of plasma membrane protrusions in cancer epithelial HeLa cells.Molecular biology reports · 2021Article
- Review
- Review
- Identifying conserved molecular targets required for cell migration of glioblastoma cancer stem cells.Cell death & disease · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
Cdc42 is a Rho-GTPase which plays a major role in regulating cell polarity and migration by specifying the localization of filopodia. However, the role of Cdc42 in GBM invasion has not been thoroughly investigated. We generated stable doxycycline-inducible clones expressing wild type (WT)-, constitutively active (CA)-, and dominant negative (DN)-Cdc42 in three different human glioma cell lines. Expression of CA-Cdc42 significantly increased the migration and invasive properties of malignant glioma cells compared to WT and DN-Cdc42 cell clones, and this was accompanied by a greater number of filopodia and focal adhesion structures which co-localize with phosphorylated focal adhesion kinase (FAK). By mass spectrometry and immunoprecipitation studies, we demonstrated that activated Cdc42 binds to IQGAP1. When implanted orthotopically in mice, the CA-Cdc42 expressing glioma cells exhibited enhanced local migration and invasion, and led to larger tumors, which significantly reduced survival. Using the Cancer Genome Atlas dataset, we determined that high Cdc42 expression is associated with poorer progression free survival, and that Cdc42 expression is highest in the proneural and neural subgroups of GBM. In summary, our studies demonstrate that activated Cdc42 is a critical determinant of the migratory and invasive phenotype of malignant gliomas, and that its effect may be mediated, at least in part, through its interaction with IQGAP1 and phosphorylated FAK.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.