Multi-omics analyses reveal BPA accelerates glioma progression via cell cycle dysregulation

Bisphenol A (BPA), a pervasive environmental endocrine disruptor, its role in glioma progression is unclear. We sought to elucidate how BPA influences glioma malignancy by integrating multi-omics analyses with experimental validation. Candidate targets of BPA were gathered from the ChEMBL database and predicted using the SwissTargetPrediction and Similarity Ensemble Approach (SEA) tools. Glioma-associated genes were identified based on Gene Expression Omnibus (GEO) datasets. Machine learning models were constructed to evaluate the diagnostic potential of these hub genes, while molecular docking was performed to assess BPA-target protein interactions. Single-cell RNA sequencing (scRNA-seq) data were leveraged to define the cellular context of BPA action. Key findings were further verified through in vitro and in vivo experiments. Our results demonstrate that BPA promotes glioma progression by exhibiting potential binding interactions with cell cycle-related proteins, thereby enhancing the proliferative capacity of glioma cells. This study provides novel mechanistic insights into the role of environmental pollutants in driving glioma pathogenesis and highlights the potential health risks associated with BPA exposure.