Nicotine: specific role in angiogenesis, proliferation and apoptosis

Abstract

Nowadays, tobacco smoking is the cause of ~5–6 million deaths per year, counting 31% and 6% of all cancer deaths (affecting 18 different organs) in middle-aged men and women, respectively. Nicotine is the addictive component of tobacco acting on neuronal nicotinic receptors (nAChR). Functional nAChR, are also present on endothelial, haematological and epithelial cells. Although nicotine itself is regularly not referred to as a carcinogen, there is an ongoing debate whether nicotine functions as a ‘tumour promoter’. Nicotine, with its specific binding to nAChR, deregulates essential biological processes like regulation of cell proliferation, apoptosis, migration, invasion, angiogenesis, inflammation and cell-mediated immunity in a wide variety of cells including foetal (regulation of development), embryonic and adult stem cells, adult tissues as well as cancer cells. Nicotine seems involved in fundamental aspects of the biology of malignant diseases, as well as of neurodegeneration. Investigating the biological effects of nicotine may provide new tools for therapeutic interventions and for the understanding of neurodegenerative diseases and tumour biology.

Keywords::

• nAChR
• apoptosis
• angiogenesis
• cancer
• cell proliferation
• neuronal diseases
• Alzheimer
• Parkinson
• Prions
• non-neuronal cells

Acknowledgements

We apologize to the many contributors of this field whose work is important but that we were unable to cite here. This mini-review undoubtedly and regrettably does not include many excellent papers in the literature regarding the peripheral expression of nAChR. We would like to thank Dr. Arch. Giulio Alzetta who helped us in drawing Figure 1.

Declaration of interest

The authors report no declarations of interest.