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The mechanism underlying arsenic-induced PD-L1 upregulation in transformed BEAS-2B cells

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机构: [1]Department of Biochemistry, College of Medicine, Yichun University, Yichun, Jiangxi 336000, China. [2]Department of Clinical Medicine, Dali University, Dali, Yunnan 671003, China. [3]Department Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA [4]Department of Neurology, the First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui 230001, China.
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Chronic exposure to arsenic promotes lung cancer. Human studies have identified immunosuppression as a risk factor for cancer development. The immune checkpoint pathway of Programmed cell death 1 ligand (PD-L1) and its receptor (programmed cell death receptor 1, PD-1) is the most studied mechanism of immunosuppression. We have previously shown that prolonged arsenic exposure induced cell transformation of BEAS-2B cells, a human lung epithelial cell line. More recently our study further showed that arsenic induced PD-L1 up-regulation, inhibited T cell effector function, and enhanced lung tumor formation in the mice. In the current study, using arsenic-induced BEAS-2B transformation as a model system we investigated the mechanism underlying PD-L1 up-regulation by arsenic. Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.Copyright © 2021. Published by Elsevier Inc.

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出版当年[2022]版:
大类 | 3 区 医学
小类 | 2 区 毒理学 2 区 药学
最新[2023]版:
大类 | 3 区 医学
小类 | 2 区 毒理学 3 区 药学
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第一作者机构: [1]Department of Biochemistry, College of Medicine, Yichun University, Yichun, Jiangxi 336000, China.
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