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      Nicotinic acetylcholine receptors and cancer

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      Author(s): , ,
      Publication date (Electronic):
      Journal: Biomedical Reports
      Publisher: D.A. Spandidos
      Keywords: nicotinic acetylcholine receptor, cancer, tobacco

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          Abstract

          Nicotine, the primary addictive constituent of cigarettes, is believed to contribute to cancer promotion and progression through the activation of nicotinic acetylcholine receptors (nAChRs), which are membrane ligand-gated cation channels. nAChRs activation can be triggered by the neurotransmitter Ach, or certain other biological compounds, such as nicotine. In recent years, genome-wide association studies have indicated that allelic variation in the α5-α3-β4 nAChR cluster on chromosome 15q24-15q25.1 is associated with lung cancer risk. The role of nAChRs in other types of cancer has also been reported. The present review highlights the role of nAChRs in types of human cancer.

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          Mammalian nicotinic acetylcholine receptors: from structure to function.

          Edson Albuquerque, Edna Pereira, Manickavasagom Alkondon … (2009)
          The classical studies of nicotine by Langley at the turn of the 20th century introduced the concept of a "receptive substance," from which the idea of a "receptor" came to light. Subsequent studies aided by the Torpedo electric organ, a rich source of muscle-type nicotinic receptors (nAChRs), and the discovery of alpha-bungarotoxin, a snake toxin that binds pseudo-irreversibly to the muscle nAChR, resulted in the muscle nAChR being the best characterized ligand-gated ion channel hitherto. With the advancement of functional and genetic studies in the late 1980s, the existence of nAChRs in the mammalian brain was confirmed and the realization that the numerous nAChR subtypes contribute to the psychoactive properties of nicotine and other drugs of abuse and to the neuropathology of various diseases, including Alzheimer's, Parkinson's, and schizophrenia, has since emerged. This review provides a comprehensive overview of these findings and the more recent revelations of the impact that the rich diversity in function and expression of this receptor family has on neuronal and nonneuronal cells throughout the body. Despite these numerous developments, our understanding of the contributions of specific neuronal nAChR subtypes to the many facets of physiology throughout the body remains in its infancy.
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            Genome-wide association scan of tag SNPs identifies a susceptibility locus for lung cancer at 15q25.1.

            Christopher Amos, Xifeng Wu, Peter Broderick … (2008)
            To identify risk variants for lung cancer, we conducted a multistage genome-wide association study. In the discovery phase, we analyzed 315,450 tagging SNPs in 1,154 current and former (ever) smoking cases of European ancestry and 1,137 frequency-matched, ever-smoking controls from Houston, Texas. For replication, we evaluated the ten SNPs most significantly associated with lung cancer in an additional 711 cases and 632 controls from Texas and 2,013 cases and 3,062 controls from the UK. Two SNPs, rs1051730 and rs8034191, mapping to a region of strong linkage disequilibrium within 15q25.1 containing PSMA4 and the nicotinic acetylcholine receptor subunit genes CHRNA3 and CHRNA5, were significantly associated with risk in both replication sets. Combined analysis yielded odds ratios of 1.32 (P < 1 x 10(-17)) for both SNPs. Haplotype analysis was consistent with there being a single risk variant in this region. We conclude that variation in a region of 15q25.1 containing nicotinic acetylcholine receptors genes contributes to lung cancer risk.
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              A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25.

              Rayjean Hung, James McKay, Valérie Gaborieau … (2008)
              Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomed Rep
                Journal ID (iso-abbrev): Biomed Rep
                Journal ID (publisher-id): BR
                Title: Biomedical Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 2049-9434
                ISSN (Electronic): 2049-9442
                Publication date (Print): May 2016
                Publication date (Electronic): 07 March 2016
                Publication date PMC-release: 07 March 2016
                Volume: 4
                Issue: 5
                Pages: 515-518
                Affiliations
                Department of Dermatology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China
                Author notes
                Correspondence to: Dr Ningning Dang, Department of Dermatology, Jinan Central Hospital Affiliated to Shandong University, 105 Jiefang Road, Jinan, Shandong 250013, P.R. China, E-mail: ningningdangxj@ 123456sina.com
                Article
                Publisher ID: BR-0-0-625
                DOI: 10.3892/br.2016.625
                PMC ID: 4840641
                PubMed ID: 27123240
                SO-VID: 32fe471b-a559-434e-9e15-be553ab52fab
                Copyright © Copyright: © Dang et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 11 November 2015
                Date accepted : 01 March 2016
                Categories
                Subject: Review

                Keywords: nicotinic acetylcholine receptor,cancer,tobacco
                Data availability:
                Keywords: nicotinic acetylcholine receptor, cancer, tobacco

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