Aim: 

The 'neuronal' nicotinic receptors (nAChRs) are also expressed in non neuronal tissues, including tumours such as small and non small cell lung cancer (NSCLC) cells. In cancer cells, nAChR activation stimulates Ca²⁺ influx, which triggers the release of growth factors that stimulate proliferation, inhibit apoptosis and stimulate angiogenesis. Moreover, several tobacco-specific carcinogenic nitrosamines bind with high affinity to homopentameric or heteropentameric nAChRs.These observations are suggestive considering that smoking is a risk factor for cancer, especially in the lung.

Methods: 

We studied the expression of nAChRs in a human NSCLC cell line (A549), by using the whole-cell configuration of the patch-clamp method. Cells were grown in RPMI medium, at 37°C. During the experiments, cells were maintained in a physiological saline solution, at room temperature. Pipettes contained a K-aspartate solution, buffered at pH 7.3.

Results and Discussion: 

The A 549 cells' resting potential was around -10 mV. At -60 mV, application of 100 microM nicotine consistently elicited inward desensitizing currents. In about half of the cells, around 90% block of the nicotinic currents was exerted by 10 nM methyllycaconitine (specific for homomeric nAChRs). In the remaining cells, mixed inhibition profiles were observed and significant block was produced by 1 microM dihydro-beta-erythroidine (specific for heteromeric nAChRs). Therefore, NSCLC cells present functional surface expression of homo- and heteromeric nAChRs.