GSBS Student Publications


Nicotinic acetylcholine receptor-mediated mechanisms in lung cancer

Student Author(s)

Ma. Reina D. Improgo

GSBS Program


UMMS Affiliation

Department of Psychiatry



Document Type


Medical Subject Headings

Animals; Autocrine Communication; Calcium; Cell Proliferation; Humans; Lung; Lung Neoplasms; Nicotine; Nicotinic Antagonists; Receptors, Nicotinic; Signal Transduction


Life Sciences | Medicine and Health Sciences | Neuroscience and Neurobiology | Psychiatry


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.

Rights and Permissions

Citation: Biochem Pharmacol. 2011 Oct 15;82(8):1015-21. Epub 2011 May 27. Link to article on publisher's site

DOI of Published Version


Related Resources

Link to Article in PubMed

Journal Title

Biochemical pharmacology

PubMed ID