Network toxicology and molecular docking analysis reveal key targets in benzopyrene-induced oral squamous cell carcinoma

Abstract Oral squamous cell carcinoma (OSCC) is one of the most common malignancies worldwide, with benzopyrene (BaP) being a crucial environmental carcinogen in its pathogenesis. However, the comprehensive molecular mechanisms underlying BaP-induced OSCC remain unclear. In this study, we adopted an integrated approach that combined network toxicology and molecular docking to delve into these mechanisms. We utilized multiple databases, including SwissTargetPrediction, CTD, TTD, and Genecard, to identify potential targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore the biological functions and pathways involved. Protein—protein interaction (PPI) networks were constructed to pinpoint core targets. Subsequently, molecular docking analysis was performed to validate the potential binding interactions. Our findings revealed 63 potential targets common to both BaP and OSCC. GO analysis indicated that these targets were mainly associated with xenobiotic stimulus response, membrane raft organization, and ubiquitin protein ligase binding. KEGG pathway analysis showed significant enrichment in lipid and atherosclerosis and endocrine resistance pathways. PPI network analysis identified TP53 and AKT1 as key targets. Molecular docking analysis demonstrated strong binding affinities between BaP and these proteins, with binding energies of TP53—BaP at—7.2 kcal/moL and AKT1—BaP at—8.0 kcal/moL. This research provides new insights into the molecular mechanisms of BaP—induced OSCC through the application of network toxicology and molecular docking methods, highlighting TP53 and AKT1 as potential key mediators. These results may aid in the development of novel therapeutic strategies for OSCC.