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Genome-wide association studies have linked lung cancer risk with a region of chromosome 15q25.1 containingCHRNA3,CHRNA5andCHRNB4encoding α3, α5 and β4 subunits of nicotinic acetylcholine receptors (nAChR), respectively. One of the strongest associations was observed for a non-silent single-nucleotide polymorphism at codon 398 inCHRNA5. Here, we have used pharmacological (antagonists) or genetic (RNA interference) interventions to modulate the activity ofCHRNA5in non-transformed bronchial cells and in lung cancer cell lines. In both cell types, silencingCHRNA5or inhibiting receptors containing nAChR α5 with α-conotoxin MII exerted a nicotine-like effect, with increased motility and invasivenessin vitroand increasing calcium influx. The effects on motility were enhanced by addition of nicotine but blocked by inhibitingCHRNA7, which encodes the homopentameric receptor α7 subunit. SilencingCHRNA5also decreased the expression of cell adhesion molecules P120 and ZO-1 in lung cancer cells as well as the expression of DeltaNp63α in squamous cell carcinoma cell lines. These results demonstrate a role forCHRNA5in modulating adhesion and motility in bronchial cells, as well as in regulating p63, a potential oncogene in squamous cell carcinoma.

carcinogenesis

CHRNA5               as negative regulator of nicotine signaling in normal and cancer bronchial cells: effects on motility, migration and p63 expression