Niller, Hans Helmut and Ay, Eva and Banati, Ferenc and Demcsak, Anett and Takacs, Maria and Minarovits, Janos (2016) Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms. REVIEWS IN MEDICAL VIROLOGY, 26 (1). pp. 57-73. ISSN 1052-9276, 1099-1654
Full text not available from this repository. (Request a copy)Abstract
Hepatitis B virus (HBV) is one of the causative agents of hepatocellular carcinoma. The molecular mechanisms of tumorigenesis are complex. One of the host factors involved is apparently the long-lasting inflammatory reaction which accompanies chronic HBV infection. Although HBV lacks a typical viral oncogene, the HBx gene encoding a pleiotropic regulatory protein emerged as a major player in liver carcinogenesis. Here we review the tumorigenic functions of HBx with an emphasis on wild type and truncated HBx variants, and their role in the transcriptional dysregulation and epigenetic reprogramming of the host cell genome. We suggest that HBx acquired by the HBV genome during evolution acts like a cellular proto-onc gene that is activated by deletion during hepatocarcinogenesis. The resulting viral oncogene (v-onc gene) codes for a truncated HBx protein that facilitates tumor progression. Copyright (c) 2015 John Wiley & Sons, Ltd.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | HEPATITIS-B-VIRUS; PROTEIN INDUCES APOPTOSIS; CARCINOGEN-INDUCED HEPATOCARCINOGENESIS; DNA METHYLATION PROFILE; E-CADHERIN EXPRESSION; NF-KAPPA-B; X-PROTEIN; HEPATOCELLULAR-CARCINOMA; TRANSGENIC MICE; HEPATOMA-CELLS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Medizinische Mikrobiologie und Hygiene |
| Depositing User: | Petra Gürster |
| Date Deposited: | 01 Mar 2019 12:36 |
| Last Modified: | 03 Sep 2020 10:30 |
| URI: | https://pred.uni-regensburg.de/id/eprint/2215 |
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