ArticleOncotarget2017
Actin cytoskeleton regulator Arp2/3 complex is required for DLL1 activating Notch1 signaling to maintain the stem cell phenotype of glioma initiating cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 36 citations in OpenAlex.
- The Notch1 intracellular domain orchestrates mechanotransduction of fluid shear stress.Life science alliance · 2026Article
- Spatial heterogeneity of malignant molecular markers in glioma revealed by stereotactic biopsy.Discover oncology · 2026Article
- Arteriovenous Malformations (AVMs): Molecular Pathogenesis, Clinical Features, and Emerging Therapeutic Strategies.Biomolecules · 2025Review
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- Article
- The Arp2/3 complex enhances cell migration on elastic substrates.Molecular biology of the cell · 2023Article
- Delineating the glioblastoma stemness by genes involved in cytoskeletal rearrangements and metabolic alterations.World journal of stem cells · 2023Review
- Notch signaling pathway: a comprehensive prognostic and gene expression profile analysis in breast cancer.BMC cancer · 2022Article
- Invasion and Propagation of White Spot Syndrome Virus: Hijacking of the Cytoskeleton, Intracellular Transport Machinery, and Nuclear Import Transporters.Journal of virology · 2022Article
- MACC1-Induced Collective Migration Is Promoted by Proliferation Rather Than Single Cell Biomechanics.Cancers · 2022Article
- Overexpression of FOXD2-AS1 enhances proliferation and impairs differentiation of glioma stem cells by activating the NOTCH pathway via TAF-1.Journal of cellular and molecular medicine · 2022Article
- Cancer stem cells: a major culprit of intra-tumor heterogeneity.American journal of cancer research · 2021Review
- Glioblastoma Stem Cell-Derived Exosomes Enhance Stemness and Tumorigenicity of Glioma Cells by Transferring Notch1 Protein.Cellular and molecular neurobiology · 2020Article
- Targeting cancer stem cell pathways for cancer therapy.Signal transduction and targeted therapy · 2020Review
- Vascular mimicry: Triggers, molecular interactions and in vivo models.Advances in cancer research · 2020Review
- The Role of DLLs in Cancer: A Novel Therapeutic Target.OncoTargets and therapy · 2020Review
- Notch1 signaling pathway promotes invasion, self-renewal and growth of glioma initiating cells via modulating chemokine system CXCL12/CXCR4.Journal of experimental & clinical cancer research : CR · 2019Article
- The Cytoskeleton-A Complex Interacting Meshwork.Cells · 2019Review
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common and lethal primary intracranial tumor. Actin cytoskeleton regulator Arp2/3 complex stimulates glioma cell motility and migration, and thus triggers tumor invasion. However, little is known regarding the role of actin cytoskeleton in maintaining the stem cell phenotype. Here, we showed that Arp2/3 complex improved stem cell phenotype maintenance through sustaining the activated Notch signaling. ShRNA targeting Notch ligand Delta-like 1 (DLL1) decreased CD133 and Nestin expression, and impaired the self-renewal ability of CD133+ U87-MG and U251-MG glioma cells, indicating DLL1/Notch1 signaling promoted stem cell phenotype maintenance. Interestingly, inhibiting Arp2/3 complex also induced the similar effect of shDLL1. Silencing DLL1 in the Arp2/3 inhibited CD133+ cells did not further abrogate the stem cell phenotype, suggesting DLL1 function requires Arp2/3 complex in glioma initiating cells (GICs). However, exogenous soluble DLL1 (sDLL1) instead of endogenous DLL1 rescued the Arp2/3 inhibition-induced stem cell phenotype suppression. The underlying mechanism was that Arp2/3 inhibition impeded DLL1 vesicular transport from cytoplasm to cell membrane, which resulted in DLL1 unable to activate Notch pathway. Furthermore, we illustrated that Arp2/3 inhibition abolished the tumorigenicity of CD133+ U87-MG neurosphere cells in the intracranial model. These findings suggested that cytoskeleton maintained the stem cell phenotype in GBM, which provide novel therapeutic strategy that anti-invasive targeted therapies may help eliminate GICs.
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.