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Updated: Jan 16, 2026

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma
Published on: February 22, 2015
Deciphering the carcinogenic role of benzo[a]pyrene in glioblastoma: Insights from network toxicology, single-cell
Liye Yi1, Wencai Wang1, Zhonghua Sun2
1The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Background:
Benzo[a]pyrene (BaP) is a known environmental carcinogen linked to multiple tumors, but its role in glioblastoma (GBM) remains poorly understood. This study aimed to explore BaP's tumorigenic mechanisms in GBM through an integrated approach combining network toxicology, single-cell transcriptomics, Mendelian randomization, and bibliometric analysis.
Methods:
BaP target genes were predicted using ChEMBL, SEA, and PharmMapper, and GBM-related genes were retrieved from GeneCards, OMIM, and TTD. Overlapping genes were used to construct a protein-protein interaction network in Cytoscape. Molecular docking and molecular dynamics simulations were performed to assess BaP-target interactions. Single-cell RNA-seq data (GSE131928) were analyzed to profile gene expression in GBM subpopulations. Mendelian randomization assessed causal relationships between core genes and GBM risk, and findings were validated in vitro. Bibliometric analysis tracked research trends on these genes.
Results:
31 overlapping genes were identified. TP53 was highly expressed in MES-like and AC-like malignant cells as well as CD8⁺ Tex cells. MR revealed a significant inverse association between TP53 expression and GBM risk (OR = 0.13, 95 % CI: 0.04-0.47, p = 0.002). Docking and simulation showed strong BaP-TP53 binding, confirmed by in vitro experiments. Bibliometrics indicated that TP53 research in GBM has shifted from basic mechanisms to clinical translation.
Conclusion:
BaP may drive GBM by targeting TP53, offering insights for GBM prevention and therapy.
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