| The lung tissue expresses the cholinergic system including nicotinic acetylcholine
receptors (nAChRs) which included in many physiologic and pathologic processes.
Mounting evidence revealed that these receptors have important roles in lung
carcinogenesis via modulating either stimulatory or inhibitory signaling pathways.
Among different members of nicotinic receptors family, alpha7‐subtype of nAChR
(α7nAChR) is a critical mediator involved in both inflammatory responses and
cancers. Several studies have shown that this receptor is the most powerful regulator
of responses that stimulate lung cancer processes such as proliferation, angiogenesis,
metastasis, and inhibition of apoptosis. Moreover, aside from its roles in the
regulation of cancer pathways, there is growing evidence indicating that α7nAChR
has profound impacts on lung inflammation through the cholinergic anti‐inflammatory
pathway. Regarding such diverse effects as well as the critical roles of nicotine as an
activator of α7nAChR on lung cancer pathogenesis, its modulation has emerged as a
promising target for drug developments. In this review, we aim to highlight the
detrimental as well as the possible beneficial influences of α7nAChR downstream
signaling cascades in the control of lung inflammation and cancer‐associated
properties. Consequently, by considering the significant global burden of lung cancer,
delineating the complex influences of α7 receptors would be of great interest in
designing novel anticancer and anti‐inflammatory strategies for the patients suffering
from lung cancer. |