A network toxicology and molecular docking study predicting putative molecular targets and pathways linking bisphenol a exposure to diffuse large B-cell lymphoma.

Bisphenol A (BPA) is a pervasive environmental endocrine disruptor implicated in hormone-related cancers.However, its association with non-hormone-dependent malignancies such as Diffuse Large B-cell Lymphoma (DLBCL) remains poorly understood.This study aimed to predict the potential molecular mechanisms linking BPA exposure to DLBCL pathogenesis through an integrated approach combining network toxicology and molecular docking.We systematically identified 46 overlapping genes shared between BPA-associated targets and DLBCL-related genes. Protein-protein interaction network analysis indicate six hub genes(HSP90AB1, HSPA8, CCNA2, CDK1, LDHA, and HSPA14),with HSP90AB1 exhibiting the highest topological centrality.Functional enrichment analysis demonstrated that these genes are significantly enriched in key oncogenic signaling pathways, including the PI3K-Akt and MAPK pathways, as well as critical biological processes such as protein folding and cell cycle regulation. Molecular docking simulations further predicted the stable binding affinity between BPA and each of the six hub proteins, with binding energies below - 6.0 kcal/mol. Collectively, our computational findings suggest a putative mechanistic framework in which BPA may contribute to DLBCL development by directly interacting with and potentially dysregulating central regulatory nodes in cellular networks, particularly the molecular chaperone HSP90AB1. These predictions require experimental validation but provide a basis for future mechanistic studies.