ArticleCell death and differentiation2025
Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Semaphorin 3G (SEMA3G) is a highly selective marker of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- Leveraging single-cell and spatial omics for brain tumour insights to improve therapeutic strategies.Molecular brain · 2026Review
- Glioblastoma Stem Cells and Tumour Microenvironment: Interactions Across Hypoxia, Vasculature and Immune Modulation.International journal of molecular sciences · 2026Review
- Vascular endothelial cells as signaling niches for epithelial stem cells in the skin.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The poor prognosis of glioblastoma (GBM) patients is attributed mainly to abundant neovascularization and presence of glioblastoma stem cells (GSCs). GSCs are preferentially localized to the perivascular niche to maintain stemness. However, the effect of abnormal communication between endothelial cells (ECs) and GSCs on GBM progression remains unknown. Here, we reveal that ECs-derived SEMA3G, which is aberrantly expressed in GBM patients, impairs GSCs by inducing c-Myc degradation. SEMA3G activates NRP2/PLXNA1 in a paracrine manner, subsequently inducing the inactivation of Cdc42 and dissociation of Cdc42 and WWP2 in GSCs. Once released, WWP2 interacts with c-Myc and mediates c-Myc degradation via ubiquitination. Genetic deletion of Sema3G in ECs accelerates GBM growth, whereas SEMA3G overexpression or recombinant SEMA3G protein prolongs the survival of GBM bearing mice. These findings illustrate that ECs play an intrinsic inhibitory role in GSCs stemness via the SMEA3G-c-Myc distal regulation paradigm. Targeting SEMA3G signaling may have promising therapeutic benefits for GBM patients.
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