Abstract:
:Epstein-Barr virus (EBV) latent infection is a critical event in nasopharyngeal carcinoma (NPC) tumorigenesis. EBV-encoded genes have been shown to be involved in immune evasion and in the regulation of various cellular signaling cascades. To elucidate the roles of EBV in NPC development, stable infection of EBV in nasopharyngeal epithelial cell lines was established. Similar to primary tumors of NPC, these infected cells exhibited a type II EBV latency expression pattern. In this study, multiple cellular signaling pathways in EBV-infected cells were investigated. We first demonstrated that in vitro EBV infection resulted in the activation of STAT3 and NFkappaB signal cascades in nasopharyngeal epithelial cells. Increased expression of their downstream targets (c-Myc, Bcl-xL, IL-6, LIF, SOCS-1, SOCS-3, VEGF, and COX-2) was also observed. Moreover, EBV latent infection induced the suppression of p38-MAPK activities, but did not activate PKR cascade. Our findings suggest that EBV latent infection is able to manipulate multiple cellular signal cascades to protect infected cells from immunologic attack and to facilitate cancer development.
journal_name
Neoplasiajournal_title
Neoplasia (New York, N.Y.)authors
Lo AK,Lo KW,Tsao SW,Wong HL,Hui JW,To KF,Hayward DS,Chui YL,Lau YL,Takada K,Huang DPdoi
10.1593/neo.05625subject
Has Abstractpub_date
2006-03-01 00:00:00pages
173-80issue
3eissn
1522-8002issn
1476-5586journal_volume
8pub_type
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