The impact of components of traditional and electronic cigarettes on the induction of the EMT process in lung cancer

Abstract

Lung cancer remains one of the leading causes of cancer-related mortality worldwide and is strongly associated with tobacco smoke exposure. In recent years, electronic cigarettes have gained popularity as seemingly safer alternatives to conventional cigarettes; however, their impact on tumor biology remains controversial. A central process in lung cancer progression is the epithelial–mesenchymal transition (EMT), which promotes cellular invasion, migration, and therapy resistance. This review summarizes current evidence on how nicotine, polycyclic aromatic hydrocarbons (PAHs), carbonyl compounds, and reactive oxygen species (ROS) modulate EMT through key signaling pathways, including PI3K/AKT, MAPK/ERK, Wnt/β-catenin, Notch, and HIF-1α. Moreover, it discusses the role of thermal processes during tobacco combustion and e-liquid heating in generating carcinogenic by-products. Emerging data indicate that both traditional and electronic cigarettes release bioactive agents capable of inducing EMT, thereby contributing to lung cancer pathogenesis and revealing potential therapeutic targets.