ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2019
EBV-associated gastric cancer evades T-cell immunity by PD-1/PD-L1 interactions.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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67 citing papers in PubMed, 95 citations in OpenAlex.
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- An EBNA1-YAP signaling axis drives immune escape through CD276 in EBV-associated gastric cancer.Cell death & disease · 2025Article
- Gastrointestinal cancer: molecular pathogenesis and targeted therapy.Molecular biomedicine · 2025Review
- PLOD1 promotes gastric cancer metastasis and immune escape by mediating extracellular matrix remodeling.Discover oncology · 2025Article
- Epstein-Barr virus-coded miR-BART19-3p promotes proliferation of EBV-associated gastric cancer by inhibiting GADD45B.Journal of translational medicine · 2025Article
- Therapeutic opportunities in EBV-positive gastric cancer subtypes.Therapeutic advances in medical oncology · 2025Review
- Clinical treatment strategy and follow-up of lymphoepithelioma-like carcinoma: a retrospective study.Future science OA · 2024Article
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- Copy Number Analysis of 9p24.1 in Classic Hodgkin Lymphoma Arising in Immune Deficiency/Dysregulation.Cancers · 2024Article
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- Phellinus linteus activates Treg cells via FAK to promote M2 macrophage polarization in hepatocellular carcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer.Frontiers in endocrinology · 2024Review
- The viral etiology of EBV-associated gastric cancers contributes to their unique pathology, clinical outcomes, treatment responses and immune landscape.Frontiers in immunology · 2024Review
- Exploring the Microbiome in Gastric Cancer: Assessing Potential Implications and Contextualizing Microorganisms beyondCancers · 2023Review
- Immunotherapeutic strategy in the management of gastric cancer: molecular profiles, current practice, and ongoing trials.Journal of the Egyptian National Cancer Institute · 2023Review
- Sintilimab treatment for chronic active Epstein-Barr virus infection and Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis in children.Orphanet journal of rare diseases · 2023Article
- Detection of Epstein-Barr virus infection in thymic epithelial tumors by nested PCR and Epstein-Barr-encoded RNA ISH.Infectious agents and cancer · 2023Article
7 more citing papers are in PubMed but not listed here.
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12 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundEpstein-Barr virus (EBV) is an oncogenic human herpesvirus involved in the development of around 10% of gastric cancers. The overexpression of PD-L1 is one of the features of EBV-associated gastric cancer (EBVaGC); however, the function of PD-L1 has not been studied in EBVaGC.
methodsWe used three EBVaGC cell lines, SNU719 cells, NCC24 cells, and YCCEL1 cells, to evaluate the PD-L1 expression and function in EBVaGC. Jurkat T-lymphocytes expressing PD-1 were co-cultured with NCC24 and YCCEL1 cells and the cell cycles were analyzed. To study the regulatory mechanism for PD-L1 expression, the 3'UTR of PD-L1 was sequenced, and the effect of inhibitors of the IFN-γ signaling pathway was evaluated.
resultsAll of the EBVaGC cell lines expressed PD-L1, and its expression was further enhanced by stimulation with IFN-γ. In Jurkat T-cells co-cultured with IFN-γ-stimulated NCC24 and YCCEL1 cells, the number of cells in the G0/G1 phase was significantly increased. This G0/G1 arrest was partially released by administration of anti-PD-L1 antibody. We found SNPs in PD-L1 3'UTR nucleotide sequences that were located at seed regions for microRNAs. Treatment of EBVaGC cell lines with JAK2-inhibitor, PI3K-inhibitor, and mTOR inhibitor reduced the level of PD-L1 expression to the same level as cells without IFN-γ stimulation.
conclusionsEBVaGC cells expressing high levels of PD-L1 suppress T-cell proliferation, and the IFN-γ signaling pathway is involved in the expression of PD-L1.
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