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Nucleic Acids Research 2006 34(10):3095-3106; doi:10.1093/nar/gkl389
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Published online 6 June 2006

© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article

Hepatitis B virus X protein and the estrogen receptor variant lacking exon 5 inhibit estrogen receptor signaling in hepatoma cells

Juqiang Han, Lihua Ding, Bin Yuan, Xiao Yang, Xiaohui Wang, Jiezhi Li, Qiujun Lu1, Cuifen Huang and Qinong Ye*

Beijing Institute of Biotechnology 27 Tai-Ping Lu Road, Beijing 100850, People's Republic of China 1 Beijing Institute of Radiation Medicine Beijing 100850, People's Republic of China

*To whom correspondence should be addressed. Tel: +8610 6818 0809; Fax: +8610 6824 8045; Email: yeqn{at}nic.bmi.ac.cn

Received January 27, 2006. Revised April 17, 2006. Accepted May 8, 2006.

Hepatitis B virus (HBV) X protein (HBx) is considered to play a role in the development of hepatocellular carcinoma (HCC) during HBV infection. HCC was shown to be more prevalent in men than in women. Estrogen, which exerts its biological function through estrogen receptor (ER), can inhibit HBV replication. ER{Delta}5, an ER{alpha} variant lacking exon 5, was found to be preferentially expressed in patients with HCC compared with patients with normal livers. Here, we report the biological role of ER{Delta}5 and a novel link between HBx and ER{alpha} signaling in hepatoma cells. ER{Delta}5 interacts with ER{alpha} in vitro and in vivo and functions as a dominant negative receptor. Both ER{alpha} and ER{Delta}5 associate with HBx. HBx decreases ER{alpha}-dependent transcriptional activity, and HBx and ER{Delta}5 have additive effect on suppression of ER{alpha} transactivation. The HBx deletion mutant that lacks the ER{alpha}-binding site abolishes the HBx repression of ER{alpha}. HBx, ER{alpha} and histone deacetylase 1 (HDAC1) form a ternary complex. Trichostatin A, a specific inhibitor of HDAC enzyme, can restore the transcriptional activity of ER{alpha} inhibited by HBx. Our data suggest that HBx and ER{Delta}5 may play a negative role in ER{alpha} signaling and that ER{alpha} agonists may be developed for HCC therapy.


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