<scp>EBV</scp> ‐ <scp>LMP1</scp> Promotes the Progression of Nasopharyngeal Carcinoma via <scp>TNC</scp> ‐Mediated Activation of <scp>PI3K</scp> /Akt Pathway

Nasopharyngeal carcinoma (NPC) is the most prevalent malignant tumor within the field of otolaryngology and is strongly associated with Epstein-Barr virus (EBV) infection. Among the factors linked to NPC progression, EBV-encoded LMP1 (latent membrane protein 1) serves as a primary contributor, although the underlying mechanisms remain partially understood. In this study, we employed a lentiviral system to establish a nasopharyngeal carcinoma cell line that stably expresses EBV-LMP1, thereby simulating the LMP1-positive nasopharyngeal carcinoma microenvironment. Our findings reveal that LMP1 upregulates the expression of TNC, which activates the PI3K-Akt signaling pathway, ultimately facilitating the proliferation, survival, migration, and in vivo growth of nasopharyngeal carcinoma cells. Notably, the knockdown of TNC or inhibition of PI3K-Akt signaling significantly reverses the enhancing effects of LMP1 on the malignant progression of NPC in both in vitro and in vivo contexts. Collectively, our results provide new insights into the mechanisms through which EBV-LMP1 contributes to the malignant progression of NPC and suggest potential strategic targets and a scientific foundation for the treatment of EBV-related NPC.