Abstract
Of the human solid cancers, Non-Small Cell Lung Cancer (NSCLC) and Malignant Pleural Mesothelioma (MPM) display a natural history supporting the concept that they develop from multiple preneoplastic pathways. Recently, new evidence suggested that nicotinic Acetylcholine Receptors (nAChRs) play a significant role in lung cancer predisposition and natural history. This review is based on some translational research aimed at evaluating the potential therapeutic effect of nAChR antagonists on NSCLC and MPM. The background and rationale of this approach are based on the experimental observations that: (a) NSCLC and MPM cells express nAChRs and (b) the activation of these receptors by agonists, namely nicotine, inhibits apoptosis, whereas receptor antagonists have a pro-apoptotic effect.
MeSH terms
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Allosteric Regulation
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Calcium / metabolism
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Carcinoma, Non-Small-Cell Lung / drug therapy
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Carcinoma, Non-Small-Cell Lung / genetics
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Carcinoma, Non-Small-Cell Lung / metabolism*
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Cell Line, Tumor
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Drug Delivery Systems
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Epithelial Cells / metabolism
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Humans
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Inflammation / drug therapy
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Inflammation / metabolism
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Lung / metabolism
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Mesothelioma / drug therapy
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Mesothelioma / genetics
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Mesothelioma / metabolism*
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Models, Biological
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Models, Chemical
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Neovascularization, Pathologic / chemically induced
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Neovascularization, Physiologic / drug effects
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Nicotinic Agonists / pharmacology
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Nicotinic Agonists / therapeutic use
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Nicotinic Antagonists / pharmacology*
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Nicotinic Antagonists / therapeutic use*
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Pleural Neoplasms / drug therapy
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Pleural Neoplasms / genetics
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Pleural Neoplasms / metabolism*
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Receptors, Nicotinic / drug effects
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Receptors, Nicotinic / genetics
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Receptors, Nicotinic / metabolism*
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Snake Venoms / pharmacology
Substances
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Nicotinic Agonists
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Nicotinic Antagonists
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Receptors, Nicotinic
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Snake Venoms
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Calcium