fig1

Multi-layered control of PD-L1 expression in Epstein-Barr virus-associated gastric cancer

Figure 1. The mechanisms of PD-L1 regulation in EBVaGC discussed in this review. EBV: Epstein-Barr virus; EBVaGC: EBV-associated gastric cancer; PD-L1: programmed cell death ligand 1; IFNγ: interferon gamma; TNFα: tumor necrosis factor alpha; EBER: Epstein-Barr encoding region; JAK: Janus kinase; STAT: signal transducers and activators of transcription; IRF: interferon regulatory factor 1; EBNA1: EBV nuclear antigen 1; BART: BamHI A rightward transcripts; PIAS: protein inhibitor of activated STAT 3; IκBα: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; LMP2A: latent membrane protein 2A; PTEN: phosphatase and tensin homolog; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; PI3K: phosphoinositide 3-kinase; AKT: protein kinase B; ARID1A: AT-rich interaction domain 1A; mTOR: mammalian target of rapamycin; 3ʹ-UTR: 3ʹ untranslated region; SV: structural variation; SNV: single nucleotide variation; BHRF1: BamHI fragment H rightward open reading frame 1. Created with BioRender.com

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)

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