ArticleJCI insight2023
The semaphorin 3A/neuropilin-1 pathway promotes clonogenic growth of glioblastoma via activation of TGF-β signaling.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- The Three Pillars of Glioblastoma: A Systematic Review and Novel Analysis of Multi-Omics and Clinical Data.Cells · 2024Pooled it
- Neuropilin‑1: Emerging roles in nerve‑vessel‑bone coupling during fracture repair (Review).International journal of molecular medicine · 2026Review
- NRP1 silencing induces ROS-mediated cell cycle arrest and mitochondrial apoptosis in non-small cell lung cancer via upregulation of AGER.Clinics (Sao Paulo, Brazil) · 2026Article
- Small and medium/large glioblastoma extracellular vesicles differentially regulate endothelial and mitochondrial function in blood-brain barrier and peripheral vasculature models.Journal of neuro-oncology · 2026Article
- Substitution of the SEMA3A basic domain with the VEGFBiological research · 2026Article
- NF-κB and STAT3 signaling uniquely stratify survival in female glioblastoma patients.iScience · 2026Article
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Harnessing the role of transforming growth factor-β in glioblastoma: a focus on phytochemicals.Medical oncology (Northwood, London, England) · 2025Review
- Development of an orthotopic medulloblastoma zebrafish model for rapid drug testing.Neuro-oncology · 2025Article
- "Brake" and "accelerator": revisiting tumor cell direct responses and the paradox of aggression in anti-VEGF therapy.Frontiers in immunology · 2025Review
- Emerging Therapies for Glioblastoma.Cancers · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
Abstract
Glioblastoma (GBM) is the most lethal brain cancer with a dismal prognosis. Stem-like GBM cells (GSCs) are a major driver of GBM propagation and recurrence; thus, understanding the molecular mechanisms that promote GSCs may lead to effective therapeutic approaches. Through in vitro clonogenic growth-based assays, we determined mitogenic activities of the ligand molecules that are implicated in neural development. We have identified that semaphorin 3A (Sema3A), originally known as an axon guidance molecule in the CNS, promotes clonogenic growth of GBM cells but not normal neural progenitor cells (NPCs). Mechanistically, Sema3A binds to its receptor neuropilin-1 (NRP1) and facilitates an interaction between NRP1 and TGF-β receptor 1 (TGF-βR1), which in turn leads to activation of canonical TGF-β signaling in both GSCs and NPCs. TGF-β signaling enhances self-renewal and survival of GBM tumors through induction of key stem cell factors, but it evokes cytostatic responses in NPCs. Blockage of the Sema3A/NRP1 axis via shRNA-mediated knockdown of Sema3A or NRP1 impeded clonogenic growth and TGF-β pathway activity in GSCs and inhibited tumor growth in vivo. Taken together, these findings suggest that the Sema3A/NRP1/TGF-βR1 signaling axis is a critical regulator of GSC propagation and a potential therapeutic target for GBM.
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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.