In recent years, the use of electronic cigarettes (e-cigarettes) or “vape” in which nicotine is the major component has been dramatically increasing, particularly among teenagers and young adults. This is due to a general perception that e-cigarettes are harmless to use, in particular for the cessation of tobacco smoking. Thus, a better understanding of whether e-cigarettes pose a risk to human health is urgently needed. Nicotine exposure can accelerate malignant growth of cancer cells. The important link of nicotine to cancer risk comes from genomic-wide screens that reveal the association of gene polymorphisms of some of nicotinic acetylcholine receptor (nAChR) subunits with the increased risk of lung cancer. A series of studies demonstrate that chronic nicotine exposure upregulates Ras signaling, disrupts redox state and mitigates tumor suppressor functions (such as p53), leading to perturbed cell growth restriction and further weakening of the genomic stability of lung epithelial cells. Once second event (such as loss of p53) occurs, nicotine is able to promote the colony formation of lung epithelial cells in soft agar medium. Taken together, these investigations indicate that persistent nicotine exposure stimulates mitogenic signaling pathways and perturbs the cellular surveillance, which creates a micro-environment that is in favor for lung tumorigenesis. Importantly, these studies substantiate our concerns about health risks associated with e-cigarette smoking, especially in young adults.

E-cigarettes, Nicotine, Mitogenic signaling, Genetic stability