PFOS promotes lung adenocarcinoma cell proliferation through PI3K/AKT/NF-κB mediated EMT.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are synthetic chemicals widely used in consumer and industrial sectors, with PFOS being particularly notable for its extensive applications. However, PFOS exposure has been associated with health issues, and while its biotoxicity-especially carcinogenic effects-has been documented, the specific risks and mechanisms in lung cancer remain unclear. This study investigates the effects of PFOS on lung adenocarcinoma (LUAD) cell lines and elucidates its carcinogenic mechanisms. We evaluated PFOS-induced proliferation in H1299 and A549 LUAD cells, focusing on its anti-apoptotic properties and impact on epithelial-mesenchymal transition (EMT), while also examining activation of the PI3K/AKT/NF-κB pathway and its role in apoptosis inhibition. Results show PFOS significantly promotes H1299 and A549 cell growth via anti-apoptotic effects, accelerates EMT in LUAD cells to enhance migration, and activates the PI3K/AKT/NF-κB pathway to facilitate proliferation and migration. These findings suggest PFOS exposure may exacerbate pre-existing lung conditions or induce carcinogenesis by suppressing apoptosis and activating PI3K/AKT/NF-κB signaling, providing evidence for PFOS-related carcinogenic potential in LUAD.