J Cancer 2020; 11(5):1125-1140. doi:10.7150/jca.36359 This issue

Review

Nicotinic-nAChR signaling mediates drug resistance in lung cancer

Wan-Li Cheng1, Kuan-Yuan Chen1,2, Kang-Yun Lee1,2,3, Po-Hao Feng2,3, Sheng-Ming Wu2,3✉

1. Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
2. Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, Taiwan
3. Division of Pulmonary Medicine, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan

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Citation:
Cheng WL, Chen KY, Lee KY, Feng PH, Wu SM. Nicotinic-nAChR signaling mediates drug resistance in lung cancer. J Cancer 2020; 11(5):1125-1140. doi:10.7150/jca.36359. Available from https://www.jcancer.org/v11p1125.htm

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Abstract

Lung cancer is the leading cause of cancer death worldwide. Cigarette smoking is the most common risk factor for lung carcinoma; other risks include genetic factors and exposure to radon gas, asbestos, secondhand smoke, and air pollution. Nicotine, the primary addictive constituent of cigarettes, contributes to cancer progression through activation of nicotinic acetylcholine receptors (nAChRs), which are membrane ligand-gated ion channels. Activation of nicotine/nAChR signaling is associated with lung cancer risk and drug resistance. We focused on nAChR pathways activated by nicotine and its downstream signaling involved in regulating apoptotic factors of mitochondria and drug resistance in lung cancer. Increasing evidence suggests that several sirtuins play a critical role in multiple aspects of cancer drug resistance. Thus, understanding the consequences of crosstalk between nicotine/nAChRs and sirtuin signaling pathways in the regulation of drug resistance could be a critical implication for cancer therapy.

Keywords: nicotinic acetylcholine receptor, drug resistance, mitochondria, sirtuin, lung cancer