ArticleOncotarget2016
PDGFRα depletion attenuates glioblastoma stem cells features by modulation of STAT3, RB1 and multiple oncogenic signals.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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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.
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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.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- FcγR-driven chimeric receptor T cells in cancer therapy: a novel frontier in antibody-guided immunotherapy.Cancer cell international · 2026Review
- Distinct molecular pathways leading to dosage-dependent temozolomide resistance in GBM stem cells.Cancer cell international · 2026Article
- 3D heterotypic models of glioblastoma reveal the impact of microglia on cellular organization and the production of a distinct secretome.Scientific reports · 2026Article
- Drug resistance in glioblastoma: Challenges, mechanisms and therapeutic strategies (Review).Molecular and clinical oncology · 2026Review
- Review
- Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases.International journal of molecular sciences · 2025Review
- The Adverse Impact of Tyrosine Kinase Inhibitors on Wound Healing and Repair.International wound journal · 2025Review
- Article
- Understanding the role of endothelial cells in brain tumor formation and metastasis: a proposition to be explored for better therapy.Journal of the National Cancer Center · 2023Review
- Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023Review
- Investigating the Interactions of Glioma Stem Cells in the Perivascular Niche at Single-Cell Resolution using a Microfluidic Tumor Microenvironment Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- ZNF117 regulates glioblastoma stem cell differentiation towards oligodendroglial lineage.Nature communications · 2022Article
- Exome sequencing of glioblastoma-derived cancer stem cells reveals rare clinically relevant frameshift deletion in MLLT1 gene.Cancer cell international · 2022Article
- Review
- Antiangiogenic Targets for Glioblastoma Therapy from a Pre-Clinical Approach, Using Nanoformulations.International journal of molecular sciences · 2020Review
- Tumor Development and Angiogenesis in Adult Brain Tumor: Glioblastoma.Molecular neurobiology · 2020Review
- Combined Inhibition of HDAC and EGFR Reduces Viability and Proliferation and Enhances STAT3 mRNA Expression in Glioblastoma Cells.Journal of molecular neuroscience : MN · 2019Article
- An RNA Aptamer Targeting the Receptor Tyrosine Kinase PDGFRα Induces Anti-tumor Effects through STAT3 and p53 in Glioblastoma.Molecular therapy. Nucleic acids · 2019Article
- Systematic analysis of gene expression alterations and clinical outcomes of STAT3 in cancer.Oncotarget · 2018Article
- Glucocorticoids Retain Bipotent Fibroblast Progenitors during Alveolar Septation in Mice.American journal of respiratory cell and molecular biology · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet derived growth factor receptors (PDGFRs) play an important role in tumor pathogenesis, and they are frequently overexpressed in glioblastoma (GBM). Earlier we have shown a higher protein expression of PDGFR isoforms (α and β) in peritumoral-tissue derived cancer stem cells (p-CSC) than in tumor core (c-CSC) of several GBM affected patients. In the current study, in order to assess the activity of PDGFRα/PDGF-AA signaling axis, we performed time course experiments to monitor the effects of exogenous PDGF-AA on the expression of downstream target genes in c-CSC vs p-CSC. Interestingly, in p-CSC we detected the upregulation of Y705-phosphorylated Stat3, concurrent with a decrement of Rb1 protein in its active state, within minutes of PDGF-AA addition. This finding prompted us to elucidate the role of PDGFRα in self-renewal, invasion and differentiation in p-CSC by using short hairpin RNA depletion of PDGFRα expression. Notably, in PDGFRα-depleted cells, protein analysis revealed attenuation of stemness-related and glial markers expression, alongside early activation of the neuronal marker MAP2a/b that correlated with the induction of tumor suppressor Rb1. The in vitro reduction of the invasive capacity of PDGFRα-depleted CSC as compared to parental cells correlated with the downmodulation of markers of epithelial-mesenchymal transition phenotype and angiogenesis. Surprisingly, we observed the induction of anti-apoptotic proteins and compensatory oncogenic signals such as EDN1, EDNRB, PRKCB1, PDGF-C and PDGF-D. To conclude, we hypothesize that the newly discovered PDGFRα/Stat3/Rb1 regulatory axis might represent a potential therapeutic target for GBM treatment.
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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.