ArticlemBio2026
EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Nasopharyngeal carcinoma: epidemiology, risk factors, signaling pathways, clinical features, diagnosis, and management.Molecular biomedicine · 2026Review
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Authors and funding
16 authors.
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Abstract
Epstein-Barr virus (EBV) latent infection is causally linked to several epithelial cancers, including endemic forms of undifferentiated nasopharyngeal carcinoma (NPC), and to a subtype of gastric cancer (GC). EBNA1 is the virus-encoded sequence-specific DNA-binding protein required for episome maintenance but also contributes to host-cell survival through multiple mechanisms, including binding to the host chromosome. We previously developed small-molecule inhibitors of EBNA1 DNA-binding that block host cell cycle progression and growth of EBV+ cell lines and tumor models IMPORTANCE: EBNA1 is essential for Epstein-Barr virus (EBV) latency and tumorigenesis, but its mechanism of action on host gene expression is not yet known. Small-molecule inhibitors of EBNA1 DNA-binding block cell cycle progression and inhibit the growth of EBV+ tumors. In this study, we use the EBNA1 small-molecule inhibitor VK1727 to identify cellular gene targets that are bound by EBNA1 and deregulated by its pharmacological inhibition in EBV+ epithelial cancer cell lines and an NPC patient-derived xenograft mouse model. We identify cell cycle-dependent kinase CDC7 and the stem cell transcription factor POU2F1 as EBNA1-bound and regulated genes important for EBV epithelial cancer proliferation. These findings not only decipher the molecular mechanism by which VK1727 blocks cell cycle progression and inhibits cell proliferation but also provide two new cellular gene targets and pathways for therapeutic intervention in EBV+ epithelial cancers.
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