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Schuller. J Cancer Metastasis Treat 2017;3:71-7 Journal of
DOI: 10.20517/2394-4722.2017.18
Cancer Metastasis and Treatment

www.jcmtjournal.com
Commentary Open Access

A new twist to neurotransmitter receptors

and cancer

Hildegard M. Schuller

Experimental Oncology Laboratory, Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee,
Knoxville, TN 37996, USA.

Correspondence to: Prof. Hildegard M. Schuller, Experimental Oncology Laboratory, Department of Biomedical and Diagnostic Sciences, College
of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA. E-mail: hmsch@utk.edu
How to cite this article: Schuller HM. A new twist to neurotransmitter receptors and cancer. J Cancer Metasta Treat 2017;3:71-7.

Article history: Received: 08-03-2017 Accepted: 26-04-2017 Published: 28-04-2017

BACKGROUND mediated neurotransmitter release by the central
and peripheral nervous system, their role in memory,
Nicotinic acetylcholine receptors (nAChRs) and beta- cognition and stress responses and the nAChR-
adrenergic receptors (β-ARs) are cell membrane mediated mechanisms of nicotine addiction have been
receptors expressed in most mammalian cells extensively studied. [1,2]
where they function as the recipients of signals
from the autonomic nervous system that maintains Beta-adrenergic receptors are coupled to the
physiological homeostasis in the mammalian organism stimulatory G-protein G that activates the enzyme
s
and regulates cell and organ responses to endogenous adenylyl cyclase (AC) upon binding of an agonist to the
and exogenous signals. The neurotransmitter of the receptor, leading to the formation of intracellular cyclic
parasympathetic branch of the autonomic nervous adenosine monophosphate (cAMP) that activates
protein kinase A (PKA) and numerous PKA-dependent
system, acetylcholine, binds as an agonist to all and independent intracellular signaling cascades in a
members of the nAChR family, thus opening the cell type-specific manner. In addition, β1 and β2-ARs
[3]
ligand-gated ion channel of the receptors. The can increase intracellular Ca levels by a variety of
2+
resulting depolarization of the cell membrane opens mechanisms [Figure 1], including the PKA-induced
voltage-gated Ca -channels (VOCs), allowing influx upregulation of L-type Ca -channels and release of
2+
[4]
2+
of additional Ca that triggers the release of cell Ca from intracellular stores that can also be induced
2+
2+
type-specific intracellular products via exocytosis. by the cAMP binding protein exchange factor directly
[1]
Influx of Ca is particularly high in response to activated by cAMP (Epac). Of particular importance
2+
[5]
agonist binding to the homomeric (comprised of alpha for the regulation of cancer cells is the fact that activated
subunits only) α7nAChR due to the selectivity of its PKA and/or cAMP stimulate the release of epidermal
ion channel for Ca whereas heteromeric (comprised growth factor (EGF), arachidonic acid (AA), [7,8]
2+
[6]
of alpha and non-alpha subunits) nAChRs have non- interleukins and vascular endothelial growth factor
selective ion channels. The mechanisms of nAChR- (VEGF), which jointly stimulate the development,
[9]
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