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Biochem Pharmacol. 2011 Oct 15;82(8):1015-21. doi: 10.1016/j.bcp.2011.05.020. Epub 2011 May 27.

Nicotinic acetylcholine receptor-mediated mechanisms in lung cancer.

Author information

1
Brudnick Neuropsychiatric Research Institute, Department of Psychiatry, University of Massachusetts Medical School, 303 Belmont St., Worcester, MA 01604, USA. Ma.Reina.Improgo@umassmed.edu

Abstract

Despite the known adverse health effects associated with tobacco use, over 45 million adults in the United States smoke. Cigarette smoking is the major etiologic factor associated with lung cancer. Cigarettes contain thousands of toxic chemicals, many of which are carcinogenic. Nicotine contributes directly to lung carcinogenesis through the activation of nicotinic acetylcholine receptors (nAChRs). nAChRs are ligand-gated ion channels, expressed in both normal and lung cancer cells, which mediate the proliferative, pro-survival, angiogenic, and metastatic effects of nicotine and its nitrosamine derivatives. The underlying molecular mechanisms involve increases in intracellular calcium levels and activation of cancer signal transduction pathways. In addition, acetylcholine (ACh) acts as an autocrine or paracrine growth factor in lung cancer. Other neurotransmitters and neuropeptides also activate similar growth loops. Recent genetic studies further support a role for nAChRs in the development of lung cancer. Several nAChR antagonists have been shown to inhibit lung cancer growth, suggesting that nAChRs may serve as valuable targets for biomarker-guided lung cancer interventions.

PMID:
21640716
DOI:
10.1016/j.bcp.2011.05.020
[Indexed for MEDLINE]

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