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Published on: March 3, 2023
Multiple roles of nicotine on cell proliferation and inhibition of apoptosis: implications on lung carcinogenesis
Abstract:
The genotoxic effects of tobacco carcinogens have long been recognized, the contribution of tobacco components to cancerogenesis by cell surface receptor signaling is relatively unexplored. Nicotine, the principal tobacco alkaloid, acts through nicotinic acetylcholine receptor (nAChR). nAChR are functionally present on human lung airway epithelial cells, on lung carcinoma [SCLC and NSCLC] and on mesothelioma and build a part of an autocrine-proliferative network that facilitates the growth of neoplastic cells. Different nAChR subunit gene expression patterns are expressed between NSCLC from smokers and non-smokers. Although there is no evidence that nicotine itself could induce cancer, different studies established that nicotine promotes in vivo the growth of cancer cells and the proliferation of endothelial cells suggesting that nicotine might contribute to the progression of tumors already initiated. These observations led to the hypothesis that nicotine might be playing a direct role in the promotion and progression of human lung cancers. Here, we briefly overview the role and the effects of nicotine on pulmonary cell growth and physiology and its feasible implications in lung carcinogenesis.
Insights
Nicotine, a tobacco component, may promote lung cancer progression by activating nicotinic acetylcholine receptors (nAChR) on lung cells. Further research is needed to understand nicotine's role in lung carcinogenesis.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Genotoxic effects of tobacco carcinogens are known, but the role of tobacco components in cancer via cell surface receptor signaling is underexplored.
- Nicotine, a primary tobacco alkaloid, interacts with nicotinic acetylcholine receptors (nAChR).
- nAChRs are present on human lung airway epithelial cells and lung cancer cells (SCLC, NSCLC), potentially driving neoplastic cell growth.
Purpose of the Study:
- To explore the role of nicotine and its interaction with nAChR in lung cancer promotion and progression.
- To investigate the implications of nicotine's effects on pulmonary cell growth and physiology in lung carcinogenesis.
Main Methods:
- Review of existing studies on nicotine, nAChR, and lung cell physiology.
- Analysis of nAChR subunit gene expression patterns in lung cancer from smokers versus non-smokers.
Main Results:
- Nicotinic acetylcholine receptors (nAChR) are functionally expressed on lung carcinoma cells, contributing to a proliferative network.
- Distinct nAChR subunit gene expression exists between smokers' and non-smokers' non-small cell lung cancer (NSCLC).
- While not directly carcinogenic, nicotine promotes in vivo cancer cell and endothelial cell proliferation, suggesting a role in tumor progression.
Conclusions:
- Nicotine may play a direct role in the promotion and progression of human lung cancers.
- Understanding nicotine-nAChR interactions is crucial for investigating lung carcinogenesis mechanisms.
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