Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016:2016:9650481.
doi: 10.1155/2016/9650481. Epub 2016 Feb 14.

The Oncogenic Functions of Nicotinic Acetylcholine Receptors

Yue Zhao  1
Affiliations
Review

The Oncogenic Functions of Nicotinic Acetylcholine Receptors

Yue Zhao. J Oncol. 2016.

Abstract

Nicotinic acetylcholine receptors (nAChRs) are ion channels that are expressed in the cell membrane of all mammalian cells, including cancer cells. Recent findings suggest that nAChRs not only mediate nicotine addiction in the brain but also contribute to the development and progression of cancers directly induced by nicotine and its derived carcinogenic nitrosamines whereas deregulation of the nAChRs is observed in many cancers, and genome-wide association studies (GWAS) indicate that SNPs nAChRs associate with risks of lung cancers and nicotine addiction. Emerging evidences suggest nAChRs are posited at the central regulatory loops of numerous cell growth and prosurvival signal pathways and also mediate the synthesis and release of stimulatory and inhibitory neurotransmitters induced by their agonists. Thus nAChRs mediated cell signaling plays an important role in stimulating the growth and angiogenic and neurogenic factors and mediating oncogenic signal transduction during cancer development in a cell type specific manner. In this review, we provide an integrated view of nAChRs signaling in cancer, heightening on the oncogenic properties of nAChRs that may be targeted for cancer treatment.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Differential effects of different nAChR subtypes on cell growth [21, 70, 96].
Figure 2
Figure 2
(a) Schematic model of nicotine action of YAP1 [94]. (b) Nicotine activates the positive feedback loop of PKC mediated phosphorylation of nAChR [97].
See this image and copyright information in PMC

References

    1. Wessler I., Kirkpatrick C. J. Acetylcholine beyond neurons: the non-neuronal cholinergic system in humans. British Journal of Pharmacology. 2008;154(8):1558–1571. doi: 10.1038/bjp.2008.185. - DOI - PMC - PubMed
    1. Sobel A., Weber M., Changeux J. P. Large-scale purification of the acetylcholine-receptor protein in its membrane-bound and detergent-extracted forms from Torpedo marmorata electric organ. European Journal of Biochemistry. 1977;80(1):215–224. doi: 10.1111/j.1432-1033.1977.tb11874.x. - DOI - PubMed
    1. O'Brien R. D., Eldefrawi M. E., Eldefrawi A. T. Isolation of acetylcholine receptors. Annual Review of Pharmacology. 1972;12:19–34. doi: 10.1146/annurev.pa.12.040172.000315. - DOI - PubMed
    1. Karlin A. The acetylcholine receptor: progress report. Life Sciences. 1974;14(8):1385–1415. doi: 10.1016/0024-3205(74)90150-7. - DOI - PubMed
    1. Galzi J.-L., Revah F., Bessis A., Changeux J.-P. Functional architecture of the nicotinic acetylcholine receptor: from electric organ to brain. Annual Review of Pharmacology and Toxicology. 1991;31(1):37–72. doi: 10.1146/annurev.pa.31.040191.000345. - DOI - PubMed

LinkOut - more resources