ArticleBMC pharmacology & toxicology2025
Mechanisms of Bisphenol A exposure on oral squamous cell carcinoma: a multidimensional network analysis.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Bisphenol A in contemporary dentistry: from material chemistry and exposure pathways to potential clinical relevance-a comprehensive narrative review.Frontiers in dental medicine · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBisphenol A (BPA) is widely used in producing polycarbonate plastics and epoxy resins, but it may pose potential health risks to the endocrine, reproductive, and immune systems and may also promote cancer. Researchers found that BPA leaching from dental materials into saliva could pose a health risk. Evidence linking BPA to oral squamous cell carcinoma (OSCC) is insufficient, and its carcinogenic potential and role in OSCC pathogenesis warrant further exploration.
methodsWe utilized network toxicology to investigate pathogenic targets and pathways in BPA with OSCC. Molecular docking and molecular dynamics simulations explored BPAs binding efficiency and stability with core targets. Single-cell sequencing analysis was conducted to determine the expression of core targets in different cell types.
resultsNetwork toxicology revealed that BPA promotes OSCC by affecting key proteins such as prostaglandin-endoperoxide synthase 2 (PTGS2) in the neuroactive ligand-receptor interaction pathway. Molecular docking demonstrated that BPA has the strongest binding affinity to PTGS2 and Kelch-like ECH-associated protein 1 (KEAP1) (−7.6 kcal/mol), followed by binding to heat shock protein 90 alpha family class A member 1 (HSP90AA1) (−6.7 kcal/mol). Molecular dynamics simulations further confirmed the stability, and single-cell sequencing demonstrated the distribution of three core targets.
conclusionThis study explored the mechanisms of BPA exposure on OSCC, identifying PTGS2, HSP90AA1, and KEAP1 as key targets. It provides a method for assessing chemical safety and offers new insights into BPAs carcinogenic effects in dentistry, which needs re-evaluation and validation in further research. CLINICAL TRIAL NUMBER: Not applicable.
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