51. Critical role of p53 in histone deacetylase inhibitor-induced Epstein-Barr virus Zta expression
- Author
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Huey-Huey Chua, Kwok Wai Lo, Shu-Chun Tsai, Shih Shin Chang, Jen-Yang Chen, Hsin-Yi Chiu, You-Chang Lo, and Ching-Hwa Tsai
- Subjects
Herpesvirus 4, Human ,Tumor suppressor gene ,medicine.drug_class ,Immunology ,medicine.disease_cause ,Microbiology ,Virus ,Virology ,Cell Line, Tumor ,Gene expression ,medicine ,Gammaherpesvirinae ,Humans ,biology ,Histone deacetylase inhibitor ,Genetic Complementation Test ,biology.organism_classification ,Epstein–Barr virus ,Virus-Cell Interactions ,Histone Deacetylase Inhibitors ,Lytic cycle ,Insect Science ,Cancer research ,Trans-Activators ,Virus Activation ,Histone deacetylase ,Tumor Suppressor Protein p53 - Abstract
The tumor suppressor gene p53 plays a central role in the maintenance of normal cell growth and genetic integrity, while its impact on the Epstein-Barr virus (EBV) life cycle remains elusive. We found that p53 is important for histone deacetylase inhibitor-induced EBV lytic gene expression in nasopharyngeal carcinoma cells. Restoration of p53 in p53-null, EBV-infected H1299 cells augments the potential for viral lytic cycle initiation. Evidence from reporter assays demonstrated that p53 contributes to the expression of the immediate-early viral Zta gene. Further analysis indicated that the DNA-binding ability of p53 and phosphorylation of Ser392 may be critical. This study provides the first evidence that p53 is involved in the regulation of EBV lytic cycle initiation.
- Published
- 2008