HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lee, H.-H. Articles by Tsai, C.-H. Search for Related Content PubMed PubMed Citation Articles by Lee, H.-H. Articles by Tsai, C.-H. Agricola Articles by Lee, H.-H. Articles by Tsai, C.-H.

Essential role of PKC in histone deacetylase inhibitor-induced Epstein–Barr virus reactivation in nasopharyngeal carcinoma cells

¹ Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan, ROC
² Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01655, USA
³ Department of Life Science and Graduate Institute of Biomedical Sciences, National Chung Hsing University, 250 Kuo-Kuang Road, Taichung 40227, Taiwan, ROC

Correspondence
Ching-Hwa Tsai
chtsai{at}ntu.edu.tw

Histone deactylase inhibitors (HDACi) are common chemotherapeutic agents that stimulate Epstein–Barr virus (EBV) reactivation; the detailed mechanism remains obscure. In this study, it is demonstrated that PKC is required for induction of the EBV lytic cycle by HDACi. Inhibition of PKC abrogates HDACi-mediated transcriptional activation of the Zta promoter and downstream lytic gene expression. Nuclear translocation of PKC is observed following HDACi stimulation and its overexpression leads to progression of the EBV lytic cycle. Our study suggests that PKC is a crucial mediator of EBV reactivation and provides a novel insight to study the regulation of the EBV lytic cycle.