Connections of nicotine to cancer

被引:313
作者
Grando, Sergei A. [1 ,2 ,3 ,4 ]
机构
[1] Univ Calif Irvine, Dept Dermatol, Irvine, CA 92782 USA
[2] Univ Calif Irvine, Dept Biol Chem, Irvine, CA 92782 USA
[3] Univ Calif Irvine, Ctr Canc, Irvine, CA 92782 USA
[4] Univ Calif Irvine, Res Inst, Irvine, CA 92782 USA
基金
美国国家卫生研究院;
关键词
MEDIATED TOBACCO TOXICITY; FIBROBLAST GROWTH FACTOR-2; NONNEURONAL ALPHA-7-NICOTINIC RECEPTOR; PROMOTES TUMOR-GROWTH; CYTOCHROME-C RELEASE; INDUCED DNA-DAMAGE; ACETYLCHOLINE-RECEPTOR; LUNG-CANCER; CELL-PROLIFERATION; IN-VITRO;
D O I
10.1038/nrc3725
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
This Opinion article discusses emerging evidence of direct contributions of nicotine to cancer onset and growth. The list of cancers reportedly connected to nicotine is expanding and presently includes small-cell and non-small-cell lung carcinomas, as well as head and neck, gastric, pancreatic, gallbladder, liver, colon, breast, cervical, urinary bladder and kidney cancers. The mutagenic and tumour-promoting activities of nicotine may result from its ability to damage the genome, disrupt cellular metabolic processes, and facilitate growth and spreading of transformed cells. The nicotinic acetylcholine receptors (nAChRs), which are activated by nicotine, can activate several signalling pathways that can have tumorigenic effects, and these receptors might be able to be targeted for cancer therapy or prevention. There is also growing evidence that the unique genetic makeup of an individual, such as polymorphisms in genes encoding nAChR subunits, might influence the susceptibility of that individual to the pathobiological effects of nicotine. The emerging knowledge about the carcinogenic mechanisms of nicotine action should be considered during the evaluation of regulations on nicotine product manufacturing, distribution and marketing.
引用
收藏
页码:419 / 429
页数:11
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