Clinical and Molecular Epidemiology, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Italy.
Scientific Direction, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Italy.
Recent Pat Anticancer Drug Discov. 2019;14(1):39-52. doi: 10.2174/1574892814666190102122848.
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.
To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer.
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.
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.
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.
吸烟相关的发病率和死亡率是明确的。尼古丁是烟草中的成瘾成分。尼古丁通过非神经元α7 烟碱型受体诱导细胞增殖、新生血管形成、上皮间质转化，并抑制药物诱导的细胞凋亡。
了解成瘾、慢性阻塞性肺疾病和肺癌的遗传、分子和细胞生物学。
在 2018 年 7 月至 9 月期间，在以下数据库中搜索要纳入综述的论文：PubMed（http://www.ncbi.nlm.nih.gov）、Scopus（http://www.scopus.com）、EMBASE（http://www.elsevier.com/online-tools/embase）和 ISI Web of Knowledge（http://apps.webofknowledge.com/）。使用以下搜索词：“尼古丁”、“烟碱型受体”和“成瘾”或“COPD”或“肺癌”。在 clinicaltrials.gov（https://clinicaltrials.gov/）检索专利。评估所有用英文撰写的论文。还查阅了检索文章的参考文献列表，以确定上述数据库未索引的其他合格研究。报告了尼古丁在暴露于苯并[a]芘-7,8-二醇-9,10-环氧化物一小时后促进人支气管上皮细胞转化的新实验数据。
烟碱型受体变异体和烟碱型受体上调参与成瘾、慢性阻塞性肺疾病和/或肺癌。尼古丁通过α7 烟碱型受体上调诱导完全的支气管上皮细胞转化。
遗传研究强调了烟碱型受体变异体在成瘾、慢性阻塞性肺疾病和/或肺癌中的作用。未来的重要步骤将是将这些遗传发现转化为临床实践。报告了一些正在申请专利的能够帮助尼古丁依赖者戒烟的干预措施。
