Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms.
Rev Med Virol
; 26(1): 57-73, 2016 Jan.
Article
en En
| MEDLINE
| ID: mdl-26593760
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 © 2015 John Wiley & Sons, Ltd.
Texto completo:
1
Colección:
01-internacional
Tipo de estudio:
Risk_factors_studies
Idioma:
En
Revista:
Rev Med Virol
Asunto de la revista:
VIROLOGIA
Año:
2016
Tipo del documento:
Article
País de afiliación:
Alemania