Abstract
Nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection. It is also characterized by heavy infiltration with non-malignant leucocytes. The EBV-encoded latent membrane protein 1 (LMP1) is believed to play an important role in NPC pathogenesis by virtue of its ability to activate multiple cell signaling pathways which collectively promote cell proliferation and survival, angiogenesis, invasiveness, and aerobic glycolysis. LMP1 also affects cell-cell interactions, antigen presentation, and cytokine and chemokine production. Here, we discuss how LMP1 modulates local immune responses that contribute to the establishment of the NPC tumor microenvironment. We also discuss strategies for targeting the LMP1 protein as a novel therapy for EBV-driven malignancies.
Highlights
Nasopharyngeal Carcinoma (NPC) is a malignancy arising in mucosal epithelium of the nasopharynx
The anti-tumor function of the cytotoxic T lymphocytes (CTL) in NPC is believed to be suppressed by cytokines, immune checkpoint proteins, and cancer-derived exosomes present in the tumor microenvironment (TME) [10, 26, 27, 31, 40]
Through its C-terminal CTAR1 and CTAR2 domains, latent membrane protein 1 (LMP1) activates multiple signaling pathways. It regulates the expression of various downstream targets associated with cell growth, survival, epithelialmesenchymal transition (EMT), migration, invasion, aerobic glycolysis as well as immune evasion [8, 31]
Summary
Nasopharyngeal Carcinoma (NPC) is a malignancy arising in mucosal epithelium of the nasopharynx. NPC is a rare cancer in western countries but has high rates of incidence throughout Southeast Asia, southern China, and the Mediterranean basin. According to the International Agency for Cancer, approximately 129,000 new cases of NPC were reported globally in 2018. More than 70% of the new cases are reported in Southern China and Southeast Asia, while only 1.7% of cases are found in the USA [1]. Type II non-keratinizing NPC is subdivided into differentiated and undifferentiated tumors [2]. The keratinizing NPC is relatively common in the Western countries (~75%), while the non-keratinizing tumors account for more than 97% of NPC cases in Southern China and Southeast Asia. The non-keratinizing form of NPC is strongly associated with EBV infection regardless of geographical distribution, ethnic origin and local prevalence of the disease. EBV is believed to be a critical etiological factor in NPC pathogenesis [3,4,5]
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