Epstein-Barr Virus Protein Can Upregulate Cyclo-Oxygenase-2 Expression through Association with the Suppressor of Metastasis Nm23-H1

• DOI: 10.1128/jvi.80.3.1321-1331.2006
• Publication Date: 2006-01-13T13:18:00Z
• Authors: Rajeev Kaul; Subhash C. Verma; Masanao Murakami; Ke Lan; Tathagata Choudhuri; Erle S. Robertson
• Keywords: Metastasis suppressor

Previous studies have demonstrated the interaction between Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) and metastatic suppressor Nm23-H1 both in vitro vivo (C. Subramanian, M. A. Cotter II, E. S. Robertson, Nat. Med. 7:350-355, 2001). EBNA3C can reverse ability of to suppress migration Burkitt's lymphoma breast carcinoma cell lines vitro. contributes EBV-associated human cancers by regulating transcription a number cellular viral promoters targeting altering activities metastasis Nm23-H1. Cyclo-oxygenase-2 (COX-2), an inducible enzyme important inflammation, is overexpressed variety influence migration. In this report we show that modulate expression COX-2 context EBV infection transformation. The levels were consistently higher EBV-positive cells than EBV-negative cells. Additionally, upregulate promoter element luciferase reporter assays, whereas alone did not affect level response but clearly contributed additive increase when coexpressed with downstream effect was also evaluated showed prostaglandin E(2) increased there some cooperativity presence EBNA3C. majority mediated through cyclic AMP NF-kappaB sites. These suggest potential role for cancers.