TY - JOUR
T1 - The mechanism underlying arsenic-induced PD-L1 upregulation in transformed BEAS-2B cells
AU - Wang, Hongsen
AU - Li, Jiaqi
AU - Xu, Wenhua
AU - Li, Chunming
AU - Wu, Kuaiying
AU - Chen, Gang
AU - Cui, Jiajun
N1 - Publisher Copyright:
© 2021
PY - 2022/1/15
Y1 - 2022/1/15
N2 - 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.
AB - 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.
KW - Arsenic
KW - Lnc-DC
KW - Lung
KW - PD-L1
KW - STAT3
KW - Tumorigenesis
KW - lnRNA
UR - http://www.scopus.com/inward/record.url?scp=85121765241&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85121765241&partnerID=8YFLogxK
U2 - 10.1016/j.taap.2021.115845
DO - 10.1016/j.taap.2021.115845
M3 - Article
C2 - 34953898
AN - SCOPUS:85121765241
SN - 0041-008X
VL - 435
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
M1 - 115845
ER -
