Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer

Recent Pat Anticancer Drug Discov. 2019;14(1):39-52. doi: 10.2174/1574892814666190102122848.

Abstract

Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis.

Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer.

Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: "nicotine", "nicotinic receptor", and "addiction" or "COPD" or "lung cancer" were used. Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported.

Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation.

Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.

Keywords: Addiction; COPD; cancer hallmarks; genetic variant; lung cancer; nicotine; nicotinic receptor; patent..

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Lung Neoplasms / chemically induced
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / metabolism*
  • Nicotinic Antagonists / metabolism
  • Nicotinic Antagonists / pharmacology
  • Nicotinic Antagonists / therapeutic use
  • Patents as Topic
  • Pulmonary Disease, Chronic Obstructive / chemically induced
  • Pulmonary Disease, Chronic Obstructive / drug therapy
  • Pulmonary Disease, Chronic Obstructive / metabolism*
  • Receptors, Nicotinic / metabolism
  • Risk Factors
  • Smoking Cessation / methods
  • Smoking Cessation Agents / metabolism*
  • Smoking Cessation Agents / pharmacology
  • Smoking Cessation Agents / therapeutic use
  • Tobacco Smoking / drug therapy
  • Tobacco Smoking / metabolism*
  • Tobacco Use Disorder / drug therapy
  • Tobacco Use Disorder / metabolism*

Substances

  • Nicotinic Antagonists
  • Receptors, Nicotinic
  • Smoking Cessation Agents