Role of ebv-circRPMS1–p53 interaction in the proliferation and clinical progression of Epstein–Barr virus-associated gastric carcinoma

作者：Ling Yang, Meini Li, Guiming Xie, Xian Wu, Mengchun Qin, Birong Guo, Jing‐yue Zhang · 发表于：Virus Research · 年份：2025 · DOI：10.1016/j.virusres.2025.199617 · 被引用次数：1 · 研究领域：Circular RNAs in diseases、Viral-associated cancers and disorders、Cancer Mechanisms and Therapy

BACKGROUND: Epstein-Barr virus-associated gastric carcinoma (EBVaGC) represents a distinct clinicopathological entity with unique molecular characteristics, including latent EBV infection and dysregulation of host tumor suppressors. However, the functional interplay between EBV circular RNAs (ebv-circRNAs) and p53 protein remains enigmatic. This study explored the role of ebv-circRPMS1, a previously uncharacterized ebv-circRNA, in EBVaGC pathogenesis. METHODS: To define ebv-circRPMS1-p53 interplay, siRNA knockdown (validated by RT-qPCR) modulated ebv-circRPMS1 in EBV+ cells. RIP/co-immunoprecipitation confirmed direct ebv-circRPMS1-p53 binding. EdU assays quantified proliferation. RNA-FISH/immunofluorescence mapped cytoplasmic colocalization. Xenografts evaluated in vivo tumorigenicity, while BaseScope/IHC analyzed tissues. Clinical cohort (n = 70) correlated co-expression with survival via Kaplan-Meier/Cox regression. RESULTS: This study demonstrated that ebv-circRPMS1 directly binds to p53, thereby enhancing tumor proliferation. Clinically, ebv-circRPMS1-p53 co-expression correlates with poor survival in EBVaGC patients. CONCLUSIONS: These findings unveil a novel viral strategy for subverting host tumor suppression, providing a rationale for targeting the ebv-circRPMS1-p53 axis in precision oncology.