ArticleCell death & disease2025
An EBNA1-YAP signaling axis drives immune escape through CD276 in EBV-associated gastric cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Review
- Computationally guided multi-epitope vaccine design targeting oncoprotein BZLF1, EBNA1, LMP1, and LMP2 for of EBV associated gastric cancer.Journal of the Egyptian National Cancer Institute · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical efficacy of anti-PD1 immunotherapy often yields low response rates in Epstein-Barr virus-associated gastric cancer (EBVaGC). To gain insights into immune escape mechanisms and discover critical molecules in anti-tumor immunity, we performed an immune checkpoint screening using transcriptome profiling and immunohistochemistry analyses. We identified CD276 as an independent immunosuppressive molecule that correlates with poor EBVaGC prognosis. Our in vitro and in vivo experiments demonstrate the role of CD276 in inducing T cell apoptosis and diminishing chemokine secretion, thereby dampening immune response and facilitating tumor progression. Mechanistically, we discovered that YAP/TEAD4 chromatin occupancy at CD276 regulatory regions leads to its transcriptional upregulation in EBVaGC, driven by EBNA1-stimulated MST1/2-LATS1/2-YAP signaling. Notably, in a humanized xenograft mouse model, EBVaGC with elevated CD276 levels exhibited resistance to anti-PD1 immunotherapy, while targeting CD276 in combination with PD1 blockade significantly reduced tumor size. Collectively, our findings elucidate the EBNA1-YAP-CD276 axis as a novel mechanism of immune escape in EBVaGC, providing insights for enhanced immunotherapeutic strategies.
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