Functionally, BPA exposure promoted prostate cancer cell invasion and EMT, which were associated with activation of the PI3K/AKT and MMP signaling pathways, whereas the PI3K inhibitor LY294002 effectively attenuated BPA-induced invasive phenotypes <i>in vitro</i> and reduced tumor progression <i>in vivo</i>.<h4>Conclusions</h4>Collectively, these findings provide mechanistic insights into BPA-driven prostate cancer progression and highlight the value of network toxicology-based approaches in environmental toxicology research. The gene discussed is AKT1; the disease is prostate carcinoma.