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Voltage-operated Calcium Channels in Small Cell Lung Carcinoma Cell Lines: Pharmacological, Functional, and Immunological Properties¹

CNR Center of Cytopharmacology, Department of Medical Pharmacology, University of Milano, via Vanvitelli 32, 20129 Milano, Italy

Different subtypes of voltage-operated calcium channels (VOCCs) are expressed in different tissues and can be distinguished by functional and pharmacological criteria. One type of high voltage-activated calcium channel, specifically recognized by the peptide neurotoxin -conotoxin (CTx), is expressed only in neurons.

Seven different human small cell lung carcinoma (SCC) cell lines were also found to bind ¹²⁵I-CTx. The binding was specific, saturable, and of high affinity.

¹²⁵I-CTx binding was not antagonized by the calcium channel ligands verapamil, nitrendipine, and diltiazem. There was a correlation between the amount of toxin binding and the detection of depolarization-induced calcium fluxes studied with the fluorimetric probe Fura2. Fura2 experiments also demonstrated that, in addition to CTx-sensitive calcium channels, SCC cell lines also expressed CTx-insensitive calcium channels, which were antagonized by nitrendipine and verapamil.

¹²⁵I-CTx-labeled VOCCs from SCC cells were, furthermore, precipitated by anti-VOCC autoantibodies obtained from patients affected by the Lambert-Eaton myasthenic syndrome, a neuromuscular disease often associated with SCC. The present findings further indicate the presence of neuronal molecules with important biological function on SCC plasma membrane and add new insights into the pathogenetic mechanism of autoimmune neurological paraneoplastic diseases, like Lambert-Eaton myasthenic syndrome.

¹ This work was partially supported by a CNR Grant: Special Project "Chimica fine."

² To whom requests for reprints should be addressed.

³ Supported by a CNR-CSIC Italian-Spanish Cooperative Treat (Grant 14.1-1989). Present address: Sloan Kettering Institute for Cancer Research, New York, NY 10021.

Received 11/ 7/89. Revised 2/16/90.

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