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 journalArticlepeer-review

4 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 languageEnglish
Article number115845
JournalToxicology and Applied Pharmacology
Volume435
DOIs
StatePublished - Jan 15 2022

Bibliographical note

Publisher Copyright:
© 2021

Keywords

  • Arsenic
  • Lnc-DC
  • Lung
  • PD-L1
  • STAT3
  • Tumorigenesis
  • lnRNA

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

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