Voltage‐sensitive calcium channels in a human small‐cell lung cancer cell line

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Abstract
Pancrazio, J.J., Oie, H.K. & Kim, Y.I. 1992. Voltage‐sensitive calcium channels in a human small‐cell lung cancer cell line.Acta Physiol Scand144, 463468. Received 1 October 1991, accepted 24 October 1991. ISSN 0001–6772. Departments of Biomedical Engineering and Neurology, University of Virginia Health Sciences Center, and the National Cancer Institute, Navy Medical Oncology Branch, Naval Hospital Bethesda, USA.Utilizing the whole‐cell patch‐clamp method we assessed the Ca2+current (Ica) in well‐established cell lines from human small‐cell carcinoma (SCC) of the lung, NCI‐H209 and NCI‐H187. The Ca2+current was readily observed in H209 tumour cells (90% of the cells tested), whereas H187 tumour cells only occasionally expressed Caz+channels (26% of the cells tested). H209 Ca2+current was evoked by potentials greater than ‐30 mV and exhibited partial inactivation over the duration of a 40 ms command potential. This inward current was unchanged by alteration of the holding potential from ‐ 80 to ‐ 40 mV and the activation phase of the Ca2+current was best fitted by Hodgkin‐Huxleym(t)2kinetics. H209 Ca2+current was reduced over 80% by verapamil (100 μM), whereas w‐conotoxin (5 μM) appeared to be without effect. In contrast, H209 Ca2+current was rapidly abolished by nifedipine (10 μm), strongly suggesting the presence of L‐type Ca2+channels. Voltage‐gated Ca2+channels may be important to the secretion of ectopic hormones and the etiology and pathogenesis of Lambert‐Eaton syndrome, an autoimmune disorder of the motor nerve terminal in which autoantibodies directed against voltage‐gated Ca2+channels are produced.