Document Detail


Transactivators Zta and Rta of Epstein-Barr virus promote G0/G1 to S transition in Raji cells: a novel relationship between lytic virus and cell cycle.
MedLine Citation:
PMID:  20338640     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study, we show that the treatment of Epstein-Barr virus (EBV) latently infected Raji cells with TPA/SB caused the cell growth arrest. The Zta-positive cells were predominantly enriched in G0/G1 phase of cell cycle. When Zta expression reached a maximal level, a fraction of Zta expressing cell population reentered S phase. Analysis of the expression pattern of a key set of cell cycle regulators revealed that the expression of Zta and Rta substantially interfered with the cell cycle regulatory machinery in Raji cells, strongly inhibiting the expression of Rb and p53 and inducing the expression of E2F1. Down-regulation of Rb was further demonstrated to be mediated by proteasomal degradation, and p53 and p21 affected at transcription level. The data indicate that both Zta and Rta promote entry into S phase of Raji cells. The important roles of Zta and Rta in EBV lytic reactivation were also demonstrated. Our finding suggests that these two transcriptional activators may act synergistically to govern the expression of downstream early and late genes as well as cellular genes and initiation of lytic cycle and manipulation of cell cycle regulatory mechanisms require the joint and interactive contributions of Rta and Zta.
Authors:
Qingwei Guo; Lu Qian; Liang Guo; Ming Shi; Changguo Chen; Xin Lv; Ming Yu; Meiru Hu; Guosheng Jiang; Ning Guo
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-24
Journal Detail:
Title:  Molecular immunology     Volume:  47     ISSN:  1872-9142     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-27     Completed Date:  2010-06-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1783-92     Citation Subset:  IM    
Copyright Information:
(c) 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Institute of Basic Medicine, Shandong Academy of Medical Science, Key Medical Laboratory for Tumor Immunology and Chinese Medicine Immunology of Shandong Province, Jinan 250062, PR China.
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MeSH Terms
Descriptor/Qualifier:
Blotting, Western
Burkitt Lymphoma / genetics,  pathology,  virology
Butyrates / pharmacology
Cell Cycle / genetics,  physiology*
Cell Line, Tumor
E2F1 Transcription Factor / genetics
Flow Cytometry
G0 Phase
G1 Phase
Gene Expression Regulation, Neoplastic / drug effects
Gene Expression Regulation, Viral / drug effects
Herpesvirus 4, Human / genetics,  physiology*
Host-Pathogen Interactions
Humans
Immediate-Early Proteins / genetics,  metabolism,  physiology*
Proteasome Endopeptidase Complex / metabolism
Retinoblastoma Protein / genetics
Reverse Transcriptase Polymerase Chain Reaction
S Phase
Tetradecanoylphorbol Acetate / pharmacology
Trans-Activators / genetics,  metabolism,  physiology*
Tumor Suppressor Protein p53 / genetics
Virus Activation
Chemical
Reg. No./Substance:
0/BRLF1 protein, Human herpesvirus 4; 0/BZLF1 protein, Herpesvirus 4, Human; 0/Butyrates; 0/E2F1 Transcription Factor; 0/E2F1 protein, human; 0/Immediate-Early Proteins; 0/Retinoblastoma Protein; 0/Trans-Activators; 0/Tumor Suppressor Protein p53; 16561-29-8/Tetradecanoylphorbol Acetate; EC 3.4.25.1/Proteasome Endopeptidase Complex

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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