ArticleFrontiers in bioinformatics2026
Integrated network toxicology, bioinformatics, and molecular docking reveal the potential molecular mechanisms linking bisphenol A to glioma progression.
Article in Frontiers in bioinformatics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Glioma is a highly aggressive central nervous system malignancy with poor clinical outcomes, and increasing attention has focused on whether environmental endocrine-disrupting chemicals contribute to its progression. This study aimed to systematically investigate the molecular mechanisms linking bisphenol A (BPA) to glioma using an integrated network toxicology and bioinformatics strategy. BPA-related targets were collected from public databases and intersected with glioma-associated genes to identify shared targets. A protein-protein interaction network was then constructed to screen hub genes, followed by transcriptomic validation using the GSE41031 dataset. Functional enrichment analyses were performed to characterize the biological processes and signaling pathways involved, and molecular docking was used to assess the binding potential of BPA with representative core targets. A total of 696 common targets were identified between BPA and glioma. Network analysis highlighted 20 hub genes, among which STAT3, AKT1, TNF, IL6, and TP53 showed the highest topological importance. Most hub genes were significantly dysregulated in glioma stem cells relative to normal neural stem cells. Enrichment analyses indicated that the shared targets were mainly associated with oxidative stress, hypoxia, xenobiotic response, steroid hormone signaling, apoptosis, focal adhesion, and the PI3K-Akt pathway. Molecular docking suggested moderate predicted binding compatibility between BPA and the five selected hub proteins. These
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