The NF-κB/IRF3 complex was enriched on the PD-L1 promoter upon UVR and was responsible for transcriptional upregulation of PD-L1. Consistently, PD-L1 levels were significantly correlated with activation of NF-κB and IRF3 gene signature in melanoma patient samples.

Jun 1, 2019 · The damage-associated molecular patterns molecule HMGB1 was secreted by melanocytes and keratinocytes upon UVR, which subsequently activated the receptor for advanced glycation endproducts (RAGE) receptor to promote NF-κB- and IRF3-dependent transcription of PD-L1 in melanocytes.

Mar 10, 2025 · Cell-intrinsic PD-L1, induced by the STING-IRF3-IFN-I axis, is identified as the driving factor for protumoral PD-L1 hi Tu.Mons. Notably, TLR2-activated Tu.Mons resist STING-induced upregulation of cell-intrinsic PD-L1 and the associated protumoral functions.

Jan 31, 2024 · The DNA translocase SMARCAL1 favors tumor immune evasion by two distinct mechanisms: it suppresses the cGAS-STING pathway by limiting endogenous DNA damage and induces PD-L1 expression by modulating chromatin accessibility at a PD-L1 regulatory element.

Jan 21, 2021 · We found that high levels of PD-L1 overexpression in EBV (+) GC were caused by focal amplification of CD274. By contrast, relatively high expression of PD-L1 in tumor tissue and infiltrating...

Oct 5, 2016 · DDRD cells demonstrated increased cytosolic DNA and constitutive activation of the viral response cGAS/STING/TBK1/IRF3 pathway. Importantly, this pathway was activated in a cell cycle-specific manner. Finally, we demonstrated that S-phase DNA damage activated expression of PD-L1 in a STING-dependent manner.

Cell-intrinsic PD-L1, induced by the STING-IRF3-IFN-I axis, is identified as the driving factor for protumoral PD-L1hiTu.Mons. Notably, TLR2-activated Tu.Mons resist STING-induced upregulation of cell-intrinsic PD-L1 and the associ-ated protumoral functions.

PD-L1 of tumor cells to induce PD-L1 in response to genomic instability, enhances anti-tumor immune responses and sensitizes tumors to immune checkpoint blockade in a mouse melanoma model. Collectively, these studies uncover SMARCAL1 as a promising target for cancer immunotherapy.

Furthermore, we demonstrated the existence of binding sites between IRF3 and PD-L1 promotors. Our data indicate that cancer cell IFIH1 promotes apoptosis and PD-L1 expression, suggesting its potential as a predictive marker of efficacy and therapeutic target in TNBC.

The DNA damage caused by RT activates the downstream ATM/ATK/Chk1 signaling pathway and is correlated with STAT3 to produce IRF3, which promotes PD-L1 expression.