Abstract
Hepatitis B virus (HBV), a major causative agent of hepatocelluar carcinoma (HCC), encodes an oncogenic X-protein (HBx) which has been known as a transcriptional transactivator on multiple viral and celluar promoters. In the report, we verified that HBx transcriptionally repress insulin-like growth factor binding protein-3 (IGFBP-3) by promoting HBx/histone deacetylase 1 (HDAC1) complex formation. HBx recruited HDAC1 forms complex with Sp1 in a p53-independent manner) and deacetylates Sp1 which resulted in the diminished binding of Sp1 on targeted DNA during transcriptional repression. Deacetylation of Sp1 by HBx recruited HDAC1 likely to be a part of the mechanism that controls HBx induced IGFBP-3 repression and the modification of chromatin structure.
Original language | English (US) |
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Pages (from-to) | 14-21 |
Number of pages | 8 |
Journal | Virus Research |
Volume | 139 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2009 |
Keywords
- Chromatin immunoprecipitation
- Histone deacetylase 1
- Immunoprecipitation
- Insulin-like growth factor binding protein-3
- Insulin-like growth factor type 1
- Trichostatin A
ASJC Scopus subject areas
- Cancer Research
- Virology
- Infectious Diseases