Shon Jin Kyung, Shon Bo Hwa, Park In Young, Lee Su Ui, Fa Liu, Chang Keun Young, Shin Je Hoon, Lee Young Ik
Liver Cell Signal Transduction Laboratory, Metabolic Syndrome Research Center, Korea Research Institute of Bioscience and Biotechnology, Liver Research Division, Lee's Biotechnology Institute of Research and Development, Taejeon 305-606, Republic of Korea.
Virus Res. 2009 Jan;139(1):14-21. doi: 10.1016/j.virusres.2008.09.006. Epub 2008 Nov 13.
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.
乙型肝炎病毒（HBV）是肝细胞癌（HCC）的主要致病因子，它编码一种致癌性X蛋白（HBx），该蛋白作为多种病毒和细胞启动子的转录反式激活因子已为人所知。在本报告中，我们证实HBx通过促进HBx/组蛋白去乙酰化酶1（HDAC1）复合物的形成来转录抑制胰岛素样生长因子结合蛋白3（IGFBP-3）。HBx招募HDAC1以不依赖p53的方式与Sp1形成复合物，并使Sp1去乙酰化，这导致在转录抑制过程中Sp1与靶向DNA的结合减少。由HBx招募的HDAC1使Sp1去乙酰化，这可能是控制HBx诱导的IGFBP-3抑制和染色质结构修饰机制的一部分。
