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- Publisher Website: 10.3390/cancers13215345
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Article: Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells
Title | Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells |
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Authors | |
Keywords | lung cancer cigarette smoke PD-L1 CHRNA7 bronchial epithelial cells |
Issue Date | 2021 |
Publisher | MDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cancers/ |
Citation | Cancers, 2021, v. 13 n. 21, p. article no. 5345 How to Cite? |
Abstract | Tobacco smoking is the top risk factor for lung cancer development. Nicotine in cigarettes can induce addiction, and its derivatives become potent carcinogens after metabolic activation and activate oncogenic signaling in lung epithelial cells through their expressed nicotinic acetylcholine receptors (nAChRs). However, the effects of smoking on the tumor immune microenvironment are under investigation. In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit α7 (nAChRα7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. The expression levels of nAChRα7 and PD-L1 in eight human bronchial epithelial cell (HBEC) lines were measured after treatment with cigarette smoke extract (CSE) or nicotine derivatives. The results showed that PD-L1 expression levels increased in HBECs after exposure to CSE or nicotine derivatives. This induction of PD-L1 expression could be diminished by treatment with CHRNA7 small-interfering RNA, and the relevant signaling was mediated via STAT3 phosphorylation and NRF2 expression. In summary, this study demonstrated that the well-known nicotine derivative-activated nAChRα7 could induce STAT3/NRF2 pathways and subsequently promote PD-L1 expression in normal lung epithelial cells. This information provides mechanistic insight into cigarette smoke-induced immune evasion in lung epithelial cells. |
Persistent Identifier | http://hdl.handle.net/10722/308273 |
ISSN | 2023 Impact Factor: 4.5 2023 SCImago Journal Rankings: 1.391 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Kwok, HH | - |
dc.contributor.author | Gao, B | - |
dc.contributor.author | Chan, KH | - |
dc.contributor.author | Ip, MSM | - |
dc.contributor.author | Minna, JD | - |
dc.contributor.author | Lam, CLD | - |
dc.date.accessioned | 2021-11-12T13:44:56Z | - |
dc.date.available | 2021-11-12T13:44:56Z | - |
dc.date.issued | 2021 | - |
dc.identifier.citation | Cancers, 2021, v. 13 n. 21, p. article no. 5345 | - |
dc.identifier.issn | 2072-6694 | - |
dc.identifier.uri | http://hdl.handle.net/10722/308273 | - |
dc.description.abstract | Tobacco smoking is the top risk factor for lung cancer development. Nicotine in cigarettes can induce addiction, and its derivatives become potent carcinogens after metabolic activation and activate oncogenic signaling in lung epithelial cells through their expressed nicotinic acetylcholine receptors (nAChRs). However, the effects of smoking on the tumor immune microenvironment are under investigation. In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit α7 (nAChRα7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. The expression levels of nAChRα7 and PD-L1 in eight human bronchial epithelial cell (HBEC) lines were measured after treatment with cigarette smoke extract (CSE) or nicotine derivatives. The results showed that PD-L1 expression levels increased in HBECs after exposure to CSE or nicotine derivatives. This induction of PD-L1 expression could be diminished by treatment with CHRNA7 small-interfering RNA, and the relevant signaling was mediated via STAT3 phosphorylation and NRF2 expression. In summary, this study demonstrated that the well-known nicotine derivative-activated nAChRα7 could induce STAT3/NRF2 pathways and subsequently promote PD-L1 expression in normal lung epithelial cells. This information provides mechanistic insight into cigarette smoke-induced immune evasion in lung epithelial cells. | - |
dc.language | eng | - |
dc.publisher | MDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cancers/ | - |
dc.relation.ispartof | Cancers | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | lung cancer | - |
dc.subject | cigarette smoke | - |
dc.subject | PD-L1 | - |
dc.subject | CHRNA7 | - |
dc.subject | bronchial epithelial cells | - |
dc.title | Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells | - |
dc.type | Article | - |
dc.identifier.email | Kwok, HH: kwokh@hku.hk | - |
dc.identifier.email | Chan, KH: koonho@hku.hk | - |
dc.identifier.email | Ip, MSM: msmip@hku.hk | - |
dc.identifier.email | Lam, CLD: dcllam@hku.hk | - |
dc.identifier.authority | Chan, KH=rp00537 | - |
dc.identifier.authority | Ip, MSM=rp00347 | - |
dc.identifier.authority | Lam, CLD=rp01345 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.3390/cancers13215345 | - |
dc.identifier.scopus | eid_2-s2.0-85117773196 | - |
dc.identifier.hkuros | 329868 | - |
dc.identifier.volume | 13 | - |
dc.identifier.issue | 21 | - |
dc.identifier.spage | article no. 5345 | - |
dc.identifier.epage | article no. 5345 | - |
dc.identifier.isi | WOS:000726588800001 | - |
dc.publisher.place | Switzerland | - |