ArticleOncogene2025
MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Epstein-Barr Virus-host epigenetic interplay: mechanisms of regulation and therapeutic potential.Clinical epigenetics · 2026Review
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Latent Epstein-Barr Virus (EBV) infection promotes cancers derived from B-lymphocytes and epithelial cells by mechanisms that largely remain unclear. EBV-encoded nuclear antigen 1 (EBNA1) is uniformly expressed in EBV-associated cancers; however, how EBNA1 contributes to cancer progression is not known. The MUC1 gene evolved in mammals to protect barrier tissues from viral infections. We report that MUC1 is upregulated in EBV-associated gastric cancers (EBVaGCs). Our results demonstrate that EBNA1 and the oncogenic MUC1-C subunit form an auto-regulatory complex that controls expression of EBNA1, MUC1-C and host cellular genes. EBNA1 appropriates MUC1-C to (i) induce DNA methyltransferase (DNMT) expression and DNA methylation, (ii) suppress CDKN1A encoding p21 to promote proliferation, and (iii) upregulate survivin to confer survival. MUC1-C is also co-opted for localization of EBNA1 in chromatin, expression of EBV latency genes and suppression of lytic genes. Targeting MUC1-C thereby induces the switch of EBV latency to activation of the lytic phase. We further demonstrate that MUC1-C is necessary for EBVaGC stem cell (CSC) state as evidenced by regulation of NOTCH stemness genes and self-renewal capacity. These findings and the demonstration that EBV positivity has no significant effect on survival of patients with GCs indicate that EBNA1 exploits MUC1-C to maintain EBV latency and that prolonged activation of MUC1-C in response to chronic EBV infection promotes EBVaGC malignant progression.
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Registered trials
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