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<p>Gliomas are highly invasive and heterogeneous tumors in the central nervous system (CNS), characterized by poor prognosis and significant therapeutic challenges. The comprehensive understanding of their molecular mechanisms remains a critical focus and challenge in current research. This study aims to integrate bioinformatics and single-cell analysis technologies to explore glioma-related cell types and immune cell infiltration features, providing new insights into the molecular pathogenesis of gliomas and identifying potential therapeutic targets. Gene expression profiles were selected from Gene Expression Omnibus (GEO), and a glioma-related gene dataset was obtained from GeneCards. Single-cell analysis was employed to identify cell types, and bioinformatics techniques were applied to identify potential pathogenic targets in gliomas. A protein–protein interaction (PPI) network was constructed, followed by functional enrichment analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Ultimately, drug target prediction and molecular docking analysis revealed the mechanisms of potential drugs. Single-cell analysis identified 10 cell types, with microglial cells and oligodendrocytes playing crucial roles in gliomas. Molecular biological analysis identified 20 key genes. GO and KEGG analyses indicated that these hub genes were primarily enriched in processes such as cellular component organization or biogenesis, cellular processes, cell junctions, and catalytic activity. The main signaling pathways involved include the p53 signaling pathway, cell cycle, and cellular senescence. Furthermore, molecular docking results showed that quercetin effectively binds to four hub targets (DLGAP5, TOP2A, CHEK1, MKI67), suggesting that quercetin may improve glioma-related biological features by acting on these targets. In conclusion, this study not only reveals the significant roles of specific cell types and key genes in gliomas but also preliminarily elucidates the molecular mechanisms of quercetin as a potential therapeutic agent, providing a solid theoretical foundation and new research directions for future glioma intervention strategies.</p>

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Identification of key biomarkers and immune microenvironment features in gliomas based on single-cell analysis combined with bioinformatics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月2日

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  • Yang Zhang,
  • Lisha Liu,
  • Chao Peng,
  • Lu Wang,
  • Jun Yang,
  • Yingjiang Gu,
  • Yu Cai

摘要

Gliomas are highly invasive and heterogeneous tumors in the central nervous system (CNS), characterized by poor prognosis and significant therapeutic challenges. The comprehensive understanding of their molecular mechanisms remains a critical focus and challenge in current research. This study aims to integrate bioinformatics and single-cell analysis technologies to explore glioma-related cell types and immune cell infiltration features, providing new insights into the molecular pathogenesis of gliomas and identifying potential therapeutic targets. Gene expression profiles were selected from Gene Expression Omnibus (GEO), and a glioma-related gene dataset was obtained from GeneCards. Single-cell analysis was employed to identify cell types, and bioinformatics techniques were applied to identify potential pathogenic targets in gliomas. A protein–protein interaction (PPI) network was constructed, followed by functional enrichment analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Ultimately, drug target prediction and molecular docking analysis revealed the mechanisms of potential drugs. Single-cell analysis identified 10 cell types, with microglial cells and oligodendrocytes playing crucial roles in gliomas. Molecular biological analysis identified 20 key genes. GO and KEGG analyses indicated that these hub genes were primarily enriched in processes such as cellular component organization or biogenesis, cellular processes, cell junctions, and catalytic activity. The main signaling pathways involved include the p53 signaling pathway, cell cycle, and cellular senescence. Furthermore, molecular docking results showed that quercetin effectively binds to four hub targets (DLGAP5, TOP2A, CHEK1, MKI67), suggesting that quercetin may improve glioma-related biological features by acting on these targets. In conclusion, this study not only reveals the significant roles of specific cell types and key genes in gliomas but also preliminarily elucidates the molecular mechanisms of quercetin as a potential therapeutic agent, providing a solid theoretical foundation and new research directions for future glioma intervention strategies.