ArticleCell death discovery2026
VK-2019 enhances gemcitabine's antitumor activity in EBV-positive nasopharyngeal carcinoma by upregulating PRODH expression.
Article in Cell death discovery, 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
Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus (EBV)-driven malignancy, making the viral protein EBNA1 a pivotal therapeutic target. This study evaluates VK-2019, a clinical-stage EBNA1 inhibitor, for its potential to sensitize NPC cells to chemotherapy. We report that VK-2019 synergistically enhances gemcitabine efficacy, reducing the IC50 by nearly 30-fold in EBV-positive C666-1 cells. Transcriptomic profiling combined with in vitro and in vivo models reveals a distinct mechanism: VK-2019 inhibition of EBNA1 downregulates c-MYC, thereby derepressing its downstream target, Proline Dehydrogenase (PRODH). Furthermore, we demonstrate that gemcitabine independently upregulates PRODH via p53 pathway activation. This dual induction of PRODH drives enhanced anti-tumor cytotoxicity. These results provide a prominent preclinical rationale for evaluating VK-2019 in combination regimens and offer a potential therapeutic strategy for patients with EBV-associated nasopharyngeal carcinoma.
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