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Nicotine upregulates the expression of alpha‐7‐nicotinic receptors on human non small cell lung cancer cells via alpha‐7‐nAChRs and protein kinase C sensitive mechanism

Cigarette smoking is strongly correlated with the onset of non‐small cell lung carcinomas (NSCLC). Nicotine, the active component of cigarettes, induces proliferation and angiogenesis via the α7‐nicotinic acetylcholine receptor (nAChR). Our study examines the effect of long‐term nicotine exposure on α7‐nAChR expression in human NSCLC cells. Chronic exposure to nicotine upregulated the level of α7‐nAChR in a dose dependent manner, with the maximal effect observed between 100nM and 10μM over a period of 12 days. The treatment of human NSCLC cell lines with 100nM nicotine produced a time‐dependent increase of expression of α7‐nAChR starting from 4 to 12 days. Most interestingly, nicotine‐induced upregulation of α7‐nAChR was reversed within 4 days of nicotine exposure; however, the increased expression of α7‐nAChR was irreversible after 12 days of nicotine treatment. Nicotine‐induced α7‐nAChR upregulation was reversed by generalized nAChR‐antagonist mecamylamine and the protein kinase C pathway. Furthermore, α7‐nAChR antagonists α‐bungarotoxin and methyllycaconitine reversed nicotine‐induced increases of α7‐nAChR expression. Our results suggest that nicotine stimulates the expression of α7‐nAChR in human NSCLC cells by an autoregulatory mechanism involving protein kinase C. Funding for our study was supported by the PhRMA Foundation and the Flight Attendant Medical Research Institute YCSA Grant.