The Impact of Lentivirus-Mediated SV2B Overexpression on Glioma Cell Proliferation, Invasion, and Migration

Objective: Glioblastoma (GBM) stands as a profoundly malignant brain tumor, often carrying a bleak prognosis. Previous investigations have highlighted the impact of the SV2B (Synaptic Vesicle Glycoprotein 2B) gene on the outcomes of GBM patients, although the specific mechanism remains unclear. This study endeavors to further explore the involvement of the SV2B gene, elucidate its related mechanisms, and bolster experimental verification. Methods: We acquired transcriptome data for gliomas from the GEO database ( https://www.ncbi.nlm.nih.gov/geo/ ) and the Chinese Glioma Genome Atlas (CCGA) database. Following this, we conducted bioinformatics analyses on the SVB2 using R (version 4.2.1) and online tools. These analyses included differential analysis, survival analysis, clinical correlation analysis, independent prognostic analysis, development of prognostic nomograms, GSEA enrichment analysis, and evaluation of immune cell infiltration.Ultimately, we confirmed that SV2B overexpression inhibits glioma progression using Western Blot, RT-qPCR, CCK-8, scratch, cell colony formation, Transwell migration, and Transwell invasion assays, as well as through subcutaneous tumor formation in mice. Results: The expression of SV2B was found to be decreased in gliomas and significantly correlated with poor patient prognosis. Down-regulation of SV2B may enhance the proliferation, migration, and invasive capabilities of glioma cells. Furthermore, SV2B expression level may independently influence the prognosis of glioma patients. A column-line graph model constructed based on this data effectively predicted the prognosis of glioma patients. Additionally, the overexpression of SV2B was shown to inhibit the proliferation, migration, and invasion abilities of GBM as demonstrated by CCK-8, cell colony, mouse subcutaneous tumorigenicity, scratch, Transwell migration, and Transwell invasion assays. GO/KEGG analysis revealed that SV2B regulates tumor proliferation, invasion, and migration processes through pathways such as ECM-receptor interaction. These mechanisms may be associated with the regulation of SYT1 protein levels by SV2B. Furthermore, SV2B and its related genes are closely associated with the tumor immune microenvironment of glioma. Conclusion: Our results underscores the crucial role of SV2B in human malignancies, with a particular emphasis on gliomas, where it promotes tumor growth and progression. Higher levels of SV2B expression are associated with worsened prognoses in these patients. Furthermore, its connection with the tumor immune microenvironment hints at its promise as both a prognostic biomarker and a therapeutic target. By shedding light on the intricate interplay between SV2B and tumorigenesis, this study offers fresh perspectives that could inform innovative approaches to the treatment and control of gliomas and other human cancers. Research Project Supported by Shanxi Scholarship Council of China, Key Research Project for High-level Science and Technology Talents in Lvliang City This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.