ArticleFrontiers in oncology2021
SNAP25 Inhibits Glioma Progression by Regulating Synapse Plasticity
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- SNARE proteins as biomarkers and therapeutic targets in central nervous system tumors.Discover oncology · 2026Review
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
- Review
- Hydroxytyrosol and Brain Tumors: Mechanisms of Action and Therapeutic Potential.Current issues in molecular biology · 2025Review
- Prognostic Role of Cuproptosis-Related Gene after Intracerebral Hemorrhage in Mice.Cellular and molecular neurobiology · 2025Article
- Brain connectivity and transcriptional changes induced by rTMS in first-episode major depressive disorder.Translational psychiatry · 2025Article
- Silibinin's role in counteracting neuronal apoptosis and synaptic dysfunction in Alzheimer's disease models.Apoptosis : an international journal on programmed cell death · 2025Article
- APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.Molecular neurodegeneration · 2025Article
- Glioma-neuron interactions: insights from neural plasticity.Frontiers in oncology · 2025Review
- Towards Effective Treatment of Glioblastoma: The Role of Combination Therapies and the Potential of Phytotherapy and Micotherapy.Current issues in molecular biology · 2024Review
- A CYCLIC PEPTIDE TARGETS GLIOBLASTOMA BY BINDING TO ABERRANTLY EXPOSED SNAP25.bioRxiv : the preprint server for biology · 2024Article
- The complex molecular epileptogenesis landscape of glioblastoma.Cell reports. Medicine · 2024Article
- Moniezia benedeni drives the SNAP-25 expression of the enteric nerves in sheep's small intestine.BMC veterinary research · 2024Article
- Cuproptosis in cancer: biological implications and therapeutic opportunities.Cellular & molecular biology letters · 2024Review
- APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.bioRxiv : the preprint server for biology · 2024Article
- Molecular subtype identification and prognosis stratification based on golgi apparatus-related genes in head and neck squamous cell carcinoma.BMC medical genomics · 2024Article
- Diffusion tensor imaging-based machine learning for IDH wild-type glioblastoma stratification to reveal the biological underpinning of radiomic features.CNS neuroscience & therapeutics · 2023Article
- Potential glioblastoma biomarkers identified by mass spectroscopy and iTRAQ labeling.Genes & diseases · 2023Article
- Identification and validation of cuproptosis related genes and signature markers in bronchopulmonary dysplasia disease using bioinformatics analysis and machine learning.BMC medical informatics and decision making · 2023Article
- Metabolic Adjustments following Glutaminase Inhibition by CB-839 in Glioblastoma Cell Lines.Cancers · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuronal activity regulated by synaptic communication exerts an important role in tumorigenesis and progression in brain tumors. Genes for soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) annotated with the function 'vesicle' about synaptic connectivity were identified, and synaptosomal-associated protein 25 (SNAP25), one of those proteins, was found to have discrepant expression levels in neuropathies. However, the specific mechanism and prognostic value of SNAP25 during glioma progression remain unclear.
methodsUsing RNA sequencing data from The Cancer Genome Atlas (TCGA) database, the differential synaptosis-related genes between low grade glioma (LGG) and glioblastoma (GBM) were identified as highly correlated. Cox proportional hazards regression analysis and survival analysis were used to differentiate the outcome of low- and high-risk patients, and the Chinese Glioma Genome Atlas (CGGA) cohort was used for validation of the data set. RT-qPCR, western blot, and immunohistochemistry assays were performed to examine the expression level of SNAP25 in glioma cells and samples. Functional assays were performed to identify the effects of SNAP25 knockdown and overexpression on cell viability, migration, and invasion. Liquid chromatography-high resolution mass spectrometry (LC-MS)-based metabolomics approach was presented for identifying crucial metabolic disturbances in glioma cells. In situ mouse xenograft model was used to investigate the role of SNAP25
resultsSNAP25 was decreased in level of expression in glioma tissues and cell lines, and low-level SNAP25 indicated an unfavorable prognosis of glioma patients. SNAP25 inhibited cell proliferation, migration, invasion and fostered glutamine metabolism of glioma cells, exerting a tumor suppressor role. Overexpressed SNAP25 exerted a lower expression level of MAP2, indicating poor neuronal plasticity and connectivity. SNAP25 could regulate glutaminase (GLS)-mediated glutaminolysis, and GLS knockdown could rescue the anti-tumor effect of SNAP25 in glioma cells. Moreover, upregulated SNAP25 also decreased tumor volume and prolonged the overall survival (OS) of the xenograft mouse.
conclusionSNAP25, a tumor suppressor inhibited carcinogenesis of glioma
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