ArticleNPJ precision oncology2026
EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells.
Article in NPJ precision oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CD73 is a metabolic immune checkpoint that regulates the homeostatic balance of adenosine levels in the tumor microenvironment (TME). However, the regulation of CD73 abnormal expression in Epstein-Barr virus (EBV)-associated malignancies remains unclear. In this study, we demonstrate that CD73 is upregulated in EBV-associated malignancies and is negatively correlated with the anti-tumor activity of NK cells. Mechanistically, EBV latent protein LMP2A upregulates CD73 through the PI3K/AKT signaling pathway, and the metabolic product of CD73, adenosine, negatively regulates the anti-tumor function of NK cells through multiple signaling pathways. Furthermore, targeted knockout of CD73, a small molecule inhibitor, or neutralizing antibody combined with the adoptive transfer of NK cells significantly improved the treatment efficacy for EBV-positive nasopharyngeal carcinoma (NPC). Importantly, we also found abnormal upregulation of CD73 in EBV-positive lymphoma, gastric cancer, and lung cancer. In summary, our research identifies the mechanism of immune evasion of NK cell anti-tumor function in EBV-associated malignancies through the abnormal expression of CD73, and targeting CD73 combined with the adoptive transfer of NK cells may provide a new strategy for immunotherapy of EBV-related malignancies.
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