ArticleScientific reports2020
The HIF1α/JMY pathway promotes glioblastoma stem-like cell invasiveness after irradiation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.Molecular oncology · 2026Article
- Expanding Microgel Parameters to Model the Tumor Microenvironment and Examine Temozolomide Resistance in Glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- Human cerebral organoids with microglia and vasculature model glioma stem cell interactions and radiotherapy response.Cell reports methods · 2026Article
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Understanding the Significance of Hypoxia-Inducible Factors (HIFs) in Glioblastoma: A Systematic Review.Cancers · 2024Review
- Alterations in Molecular Profiles Affecting Glioblastoma Resistance to Radiochemotherapy: Where Does the Good Go?Cancers · 2022Review
- Molecular Mechanisms and Clinical Challenges of Glioma Invasion.Brain sciences · 2022Review
- Abnormal migration behavior linked to Rac1 signaling contributes to primordial germ cell exhaustion in Fanconi anemia pathway-deficient Fancg-/- embryos.Human molecular genetics · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human glioblastoma (GBM) is the most common primary malignant brain tumor. A minor subpopulation of cancer cells, known as glioma stem-like cells (GSCs), are thought to play a major role in tumor relapse due to their stem cell-like properties, their high resistance to conventional treatments and their high invasion capacity. We show that ionizing radiation specifically enhances the motility and invasiveness of human GSCs through the stabilization and nuclear accumulation of the hypoxia-inducible factor 1α (HIF1α), which in turn transcriptionally activates the Junction-mediating and regulatory protein (JMY). Finally, JMY accumulates in the cytoplasm where it stimulates GSC migration via its actin nucleation-promoting activity. Targeting JMY could thus open the way to the development of new therapeutic strategies to improve the efficacy of radiotherapy and prevent glioma recurrence.
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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.