Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells

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. Alt...

Full description

Bibliographic Details
Main Authors: Chung-Chun Wu, Chih-Yeu Fang, Sheng-Yen Huang, Shih-Hsin Chiu, Chia-Huei Lee, Jen-Yang Chen
Format: Article
Language:English
Published: MDPI AG 2018-04-01
Series:Cancers
Subjects:
Online Access:http://www.mdpi.com/2072-6694/10/4/120
_version_ 1797728754313723904
author Chung-Chun Wu
Chih-Yeu Fang
Sheng-Yen Huang
Shih-Hsin Chiu
Chia-Huei Lee
Jen-Yang Chen
author_facet Chung-Chun Wu
Chih-Yeu Fang
Sheng-Yen Huang
Shih-Hsin Chiu
Chia-Huei Lee
Jen-Yang Chen
author_sort Chung-Chun Wu
collection DOAJ
description 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.
first_indexed 2024-03-12T11:19:35Z
format Article
id doaj.art-445554c8f8c948f78cffc50e8150de28
institution Directory Open Access Journal
issn 2072-6694
language English
last_indexed 2024-03-12T11:19:35Z
publishDate 2018-04-01
publisher MDPI AG
record_format Article
series Cancers
spelling doaj.art-445554c8f8c948f78cffc50e8150de282023-09-02T01:20:50ZengMDPI AGCancers2072-66942018-04-0110412010.3390/cancers10040120cancers10040120Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer CellsChung-Chun Wu0Chih-Yeu Fang1Sheng-Yen Huang2Shih-Hsin Chiu3Chia-Huei Lee4Jen-Yang Chen5National Institute of Cancer Research, National Health Research Institutes, Zhunan 350, TaiwanDepartment of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei 116, TaiwanNational Institute of Cancer Research, National Health Research Institutes, Zhunan 350, TaiwanNational Institute of Cancer Research, National Health Research Institutes, Zhunan 350, TaiwanNational Institute of Cancer Research, National Health Research Institutes, Zhunan 350, TaiwanNational Institute of Cancer Research, National Health Research Institutes, Zhunan 350, TaiwanNasopharyngeal 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.http://www.mdpi.com/2072-6694/10/4/120Epstein–Barr virusreactivationlytic cyclegenomic instabilitynasopharyngeal carcinoma
spellingShingle Chung-Chun Wu
Chih-Yeu Fang
Sheng-Yen Huang
Shih-Hsin Chiu
Chia-Huei Lee
Jen-Yang Chen
Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
Cancers
Epstein–Barr virus
reactivation
lytic cycle
genomic instability
nasopharyngeal carcinoma
title Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
title_full Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
title_fullStr Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
title_full_unstemmed Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
title_short Perspective: Contribution of Epstein–Barr virus (EBV) Reactivation to the Carcinogenicity of Nasopharyngeal Cancer Cells
title_sort perspective contribution of epstein barr virus ebv reactivation to the carcinogenicity of nasopharyngeal cancer cells
topic Epstein–Barr virus
reactivation
lytic cycle
genomic instability
nasopharyngeal carcinoma
url http://www.mdpi.com/2072-6694/10/4/120
work_keys_str_mv AT chungchunwu perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells
AT chihyeufang perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells
AT shengyenhuang perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells
AT shihhsinchiu perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells
AT chiahueilee perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells
AT jenyangchen perspectivecontributionofepsteinbarrvirusebvreactivationtothecarcinogenicityofnasopharyngealcancercells