LMP1 Promotes EV Secretion through SDC2 and SYTL4 via NF-κB Signaling in NPC Cells

Extracellular vesicles (EVs) have been increasingly recognized as key players in cancer progression and metastasis. The Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1), closely associated with nasopharyngeal carcinoma (NPC) pathogenesis, has been shown to promote EV secretion. However, the molecular mechanism underlying this process remains poorly understood.

Recent studies have highlighted the importance of SDC2 and SYTL4 in EV formation and release. SDC2 interacts with syntenin, promoting the formation of EVs, while SYTL4 is associated with the release of EVs. In the present study, we investigated the role of LMP1 in regulating EV secretion through SDC2 and SYTL4.

Our results showed that LMP1 promotes EV secretion via upregulated syndecan-2 (SDC2) and synaptotagmin-like-4 (SYTL4) through NF-κB signaling in NPC cells. These findings indicate that LMP1 plays a crucial role in regulating EV secretion, which may contribute to cancer progression and metastasis.

The significance of this study lies in its identification of the molecular mechanism by which LMP1 promotes EV secretion. Understanding the regulation of EV secretion may provide valuable insights into the development of novel therapeutic strategies for NPC treatment. Further research is needed to fully elucidate the role of LMP1 in EV-mediated cell-to-cell communication and cancer progression.

The study also highlights the importance of NF-κB signaling in regulating SDC2 and SYTL4 expression, which may have implications for the diagnosis and treatment of NPC. Overall, this study contributes to our understanding of the complex interplay between LMP1, SDC2, SYTL4, and EVs in NPC pathogenesis.

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