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

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.

Automated summary

Chronic exposure to arsenic has been linked to lung cancer. This study investigates the mechanism behind arsenic-induced up-regulation of PD-L1, a key factor in immunosuppression. Using a BEAS-2B cell transformation model, the study finds that long non-coding RNA Lnc-DC and signal transducer and activator of transcription 3 (STAT3) mediate the up-regulation of PD-L1 by arsenic.