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

Hongsen Wang; Jiaqi Li; Wenhua Xu; Chunming Li; Kuaiying Wu; Gang Chen; Jiajun Cui

doi:10.1016/j.taap.2021.115845

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

Hongsen Wang
, Jiaqi Li
, Wenhua Xu
, Chunming Li
, Kuaiying Wu
, Gang Chen
, Jiajun Cui

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

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.

Original language	English
Article number	115845
Journal	Toxicology and Applied Pharmacology
Volume	435
DOIs	https://doi.org/10.1016/j.taap.2021.115845
State	Published - Jan 15 2022

Bibliographical note

Publisher Copyright:
© 2021

Funding

This work was supported by NSFC grant 31660325 (JC) and NIH grant ES026657 (GC).

Funders	Funder number
National Institutes of Health (NIH)
National Institute of Environmental Health Sciences (NIEHS)	R01ES026657
National Natural Science Foundation of China (NSFC)	31660325

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Arsenic
Lnc-DC
Lung
PD-L1
STAT3
Tumorigenesis
lnRNA

ASJC Scopus subject areas

Toxicology
Pharmacology

Access to Document

10.1016/j.taap.2021.115845

Cite this

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title = "The mechanism underlying arsenic-induced PD-L1 upregulation in transformed BEAS-2B cells",

abstract = "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.",

keywords = "Arsenic, Lnc-DC, Lung, PD-L1, STAT3, Tumorigenesis, lnRNA",

author = "Hongsen Wang and Jiaqi Li and Wenhua Xu and Chunming Li and Kuaiying Wu and Gang Chen and Jiajun Cui",

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doi = "10.1016/j.taap.2021.115845",

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AU - Wang, Hongsen

AU - Li, Jiaqi

AU - Xu, Wenhua

AU - Li, Chunming

AU - Wu, Kuaiying

AU - Chen, Gang

AU - Cui, Jiajun

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

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SN - 0041-008X

VL - 435

JO - Toxicology and Applied Pharmacology

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M1 - 115845

ER -

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

Abstract

Bibliographical note

Funding

UN SDGs

Keywords

ASJC Scopus subject areas

Access to Document

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