ArticleBritish journal of cancer2025
LMP2A regulates S901 phosphorylation of EphA2 to maintain EBV latent infection in gastric cancer.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pseudorabies virus pUL40 drives inflammatory signaling through competitive hijacking of EphA2 from the Akt-EphA2 interaction.Veterinary research · 2026Article
- Epstein-Barr virus receptors: classification, functional mechanisms, and pathogenic implications.Journal of virology · 2026Review
- The research progress of the synergistic effect of Epstein-Barr virus andFrontiers in oncology · 2026Review
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Authors and funding
7 authors.
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Abstract
backgroundEBV infection is closely related to the occurrence and development of gastric cancer (GC). EphA2 is an important oncogenic protein in the progression of a variety of tumors. However, the relationship between EphA2 and EBV in EBV-associated GC (EBVaGC) remains unclear.
methodsImmunohistochemical and molecular experiments were performed to compare EphA2 expression between EBVaGC and EBV-negative gastric cancer (EBVnGC). The role of LMP2A in EphA2 expression was evaluated by transfection of LMP2A plasmid or siRNA. The S901 and Y772 phosphorylation site mutant plasmids of EphA2 were constructed to study their biological functions.
resultsEphA2 expression was significantly downregulated in EBVaGC tissues and cell lines. LMP2A down-regulates EphA2 expression through the PI3K/AKT signaling pathway and autophagy pathway. pS901-EphA2 and pY772-EphA2 promote the malignant function of GC cells. In addition, pS901-EphA2 promotes the lytic reactivation of EBV by activating the JNK signaling pathway.
conclusionsOur data suggests that pS901-EphA2 and pY772-EphA2 play a role in the malignant characteristics of GC, and that pS901-EphA2 induced phosphorylation of JNK is a potential mechanism by which EphA2 promotes the lytic reactivation of EBV. LMP2A is involved in EBVaGC progression and maintenance of EBV latent infection by down-regulating EphA2 expression.
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