ArticleCancers2019
Semaphorin-7A on Exosomes: A Promigratory Signal in the Glioma Microenvironment.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Carmustine Wafers Implantation in Patients With Newly Diagnosed High Grade Glioma: Is It Still an Option?Frontiers in neurology · 2022Pooled it
- Targeting Semaphorin 7a signaling in preclinical models of endocrine therapy-resistant breast cancer.Molecular cancer therapeutics · 2026Article
- Comprehensive landscape and future perspectives of exosomal circular RNAs in cardiovascular disease.Frontiers in pharmacology · 2026Review
- Semaphorin 5A modulates focal adhesion pathway and lamellipodia formation in melanoma.Cell communication and signaling : CCS · 2025Article
- Tumor-derived SEMA7A regulates fatty acid oxidation in the tumor-associated macrophages to promote the progression of non-small cell lung cancer.Frontiers in immunology · 2025Article
- Action Mechanisms of Exosomes Derived from GD3/GD2-Positive Glioma Cells in the Regulation of Phenotypes and Intracellular Signaling: Roles of Integrins.International journal of molecular sciences · 2024Article
- Glioma-Derived Exosomes and Their Application as Drug Nanoparticles.International journal of molecular sciences · 2024Review
- Exosomal TNF-α mediates voltage-gated Na+ channel 1.6 overexpression and contributes to brain tumor-induced neuronal hyperexcitability.The Journal of clinical investigation · 2024Article
- Exosomes: new targets for understanding axon guidance in the developing central nervous system.Frontiers in cell and developmental biology · 2024Review
- Tumor Microenvironment and Glioblastoma Cell Interplay as Promoters of Therapeutic Resistance.Biology · 2023Review
- Remote neuronal activity drives glioma infiltration via Sema4f.bioRxiv : the preprint server for biology · 2023Article
- The dual action of glioma-derived exosomes on neuronal activity: synchronization and disruption of synchrony.Cell death & disease · 2022Article
- Article
- Review
- Semaphorins as Potential Immune Therapeutic Targets for Cancer.Frontiers in oncology · 2022Review
- Pathophysiological roles of integrins in gliomas from the perspective of glioma stem cells.Frontiers in cell and developmental biology · 2022Review
- Exosomes and cancer immunotherapy: A review of recent cancer research.Frontiers in oncology · 2022Review
- Inhibitory Mechanism of Combined Hydroxychavicol With Epigallocatechin-3-Gallate Against Glioma Cancer Cell Lines: A Transcriptomic Analysis.Frontiers in pharmacology · 2022Article
- Microengineered perfusable 3D-bioprinted glioblastoma model for in vivo mimicry of tumor microenvironment.Science advances · 2021Article
- Anti-JMH alloantibody in inherited JMH-negative patients leads to immunogenic destruction of JMH-positive RBCs.Clinical and experimental immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Exosomes are one of the most important mediators of the cross talk occurring between glioma stem cells (GSCs) and the surrounding microenvironment. We have previously shown that exosomes released by patient-derived glioma-associated stem cells (GASC) are able to increase, in vitro, the aggressiveness of both GSC and glioblastoma cell lines. To understand which molecules are responsible for this tumour-supporting function, we performed a descriptive proteomic analysis of GASC-exosomes and identified, among the others, Semaphorin7A (SEMA7A). SEMA7A was described as a promigratory cue in physiological and pathological conditions, and we hypothesised that it could modulate GSC migratory properties. Here, we described that SEMA7A is exposed on GASC-exosomes' surface and signals to GSC through Integrin β1. This interaction activates focal adhesion kinase into GSC and increases their motility, in our patient-based in vitro model. Our findings suggest SEMA7A-β1-integrin as a new target to disrupt the communication between GSCs and the supporting microenvironment.
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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.