Abstract
Nasopharyngeal carcinoma (NPC) is a squamous cell carcinoma derived from the epithelium of the post-nasal cavity, with a unique geographic and ethnic distribution. Epstein–Barr virus (EBV) is an etiological agent of NPC, but how it contributes to carcinogenesis is not completely clear. Although it is thought that EBV latency participates in the development of NPC, increasing evidence reveals that the lytic cycle also plays an important role in the carcinogenic process. In this review, we summarize our recent studies on how EBV reactivation causes genomic instability and accelerates tumorigenesis in epithelial cells. The roles of three lytic genes, namely, BRLF1, BGLF5 and BALF3, in this process are also introduced. Moreover, blocking EBV reactivation using natural compounds may help delay the progression of NPC tumorigenesis. These studies provide a new insight into NPC carcinogenesis and raise the possibility that inhibition of EBV reactivation may be a novel approach to prevent the relapse of NPC.
Highlights
Epstein–Barr virus (EBV) infection, consumption of nitroso-compounds, and genetic factors have been implicated in the carcinogenesis of nasopharyngeal carcinoma (NPC) [1,2]
These findings suggest that EBV may contribute to the carcinogenesis of Nasopharyngeal carcinoma (NPC), including initiation and relapse
Lytic genes have been associated with EBV. Carcinogenetic effects, such as BZLF1 in lymphoblastoid cell lines [9], BCRF1 in human B lymphocytes [10], and BARF1 in gastric cancer ([11] and reviewed in [12]), fewer investigations have been conducted on the contribution of EBV lytic genes to the tumorigenesis of NPC
Summary
Epstein–Barr virus (EBV) infection, consumption of nitroso-compounds, and genetic factors have been implicated in the carcinogenesis of nasopharyngeal carcinoma (NPC) [1,2]. Individuals with high levels of antibodies against EBV have been shown to have a greater risk of NPC onset [3,4,5] These findings suggest that EBV may contribute to the carcinogenesis of NPC, including initiation and relapse. Years of study led to the proposal that latent EBV infection contributes to the carcinogenesis of NPC [6], on the basis of epidemiological studies, most adults in Taiwan are EBV carriers but only a relatively small number develop NPC. Recurrent treatment resulted in an increase in chromosome aberration and in the invasiveness and tumorigenicity of NA cells These results indicate that recurrent EBV reactivation may contribute to the accumulation of GI and promote tumorigenic progression of NPC cells
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