Moreover, we found that stimulation of EV secretion by LMP1 can enhance the proliferation and invasion ability of recipient NPC cells and tumor growth in vivo. Further study indicated that SDC2 interacted with syntenin, which promoted the formation of the EVs, and SYTL4 is associated with the release of EVs. In the present study, we found that LMP1 promotes EV secretion via upregulated syndecan-2 (SDC2) and synaptotagmin-like-4 (SYTL4) through NF-κB signaling in NPC cells. However, the molecular mechanism by which LMP1 promotes EV secretion is not well understood. Several reports have shown that LMP1 promotes EV secretion, and LMP1 trafficking by EVs can enhances cancer progression and metastasis.

The Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1), which is closely associated with nasopharyngeal carcinoma (NPC) pathogenesis, can trigger multiple cell signaling pathways that affect cell progression. Increasing evidence indicates that extracellular vesicle (EV) play an important role in cancer cell-to-cell communication.

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