Integrated study reveals molecular mechanisms by which bisphenol A promotes ovarian cancer

. Functional analysis indicated that the risk model and its constituent genes are associated with humoral immune activation and cellular immunosuppression. Furthermore, the activation of neuroactive ligand-receptor interaction signaling appears to be a common molecular mechanism through which these risk genes contribute to OC. Molecular docking, molecular dynamics simulations, and cellular experiments confirmed a stable binding interaction between BPA and the CDKN1B protein. These findings provide scientific data for a deeper understanding of the molecular mechanisms linking BPA to OC, aiding risk prediction and personalized prevention for exposed individuals.