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Voltage-operated calcium channels in small cell lung carcinoma cell lines: pharmacological, functional, and

E Sher1, A Pandiella, F Clementi

  • 1Department of Medical Pharmacology, University of Milano, Italy.

Cancer Research
|July 1, 1990
PubMed

Insights

Small cell lung carcinoma (SCC) cells express neuronal voltage-operated calcium channels (VOCCs) that bind omega-conotoxin. These channels are implicated in Lambert-Eaton myasthenic syndrome, offering insights into paraneoplastic diseases.

Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Voltage-operated calcium channels (VOCCs) exhibit diverse subtypes with tissue-specific expression.
  • Omega-conotoxin (omega CTx) specifically identifies a neuronal subtype of high voltage-activated calcium channels.

Purpose of the Study:

  • To investigate the presence and characteristics of omega CTx-sensitive VOCCs in small cell lung carcinoma (SCC) cell lines.
  • To explore the relationship between these channels and depolarization-induced calcium fluxes.
  • To examine the potential role of these channels in Lambert-Eaton myasthenic syndrome (LEMS).

Main Methods:

  • Radioligand binding assays using 125I-omega CTx to assess VOCCs in SCC cell lines.
  • Pharmacological characterization using calcium channel antagonists (verapamil, nitrendipine, diltiazem).
  • Functional analysis of depolarization-induced calcium fluxes using the Fura2 fluorimetric probe.
  • Immunoprecipitation with anti-VOCC autoantibodies from LEMS patients.

Main Results:

  • Seven human SCC cell lines demonstrated specific, saturable, high-affinity binding of 125I-omega CTx.
  • Omega CTx binding was not inhibited by verapamil, nitrendipine, or diltiazem.
  • SCC cells possess both omega CTx-sensitive and omega CTx-insensitive calcium channels.
  • A correlation was observed between omega CTx binding and calcium influx.
  • SCC VOCCs were precipitated by autoantibodies from LEMS patients.

Conclusions:

  • SCC cell lines express neuronal omega CTx-sensitive VOCCs, suggesting the presence of neuronal molecules on tumor cells.
  • These findings provide insights into the pathogenesis of autoimmune neurological paraneoplastic diseases like LEMS, often associated with SCC.
  • The study highlights the potential for targeting these channels in related paraneoplastic syndromes.

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