Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms

Hans Helmut Niller, Eva Ay, Ferenc Banati, Anett Demcsák, M. Takács, J. Mináróvits

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)57-73
Number of pages17
JournalReviews in Medical Virology
Volume26
Issue number1
DOIs
Publication statusPublished - Jan 1 2016

Fingerprint

Hepatitis B virus
Epigenomics
Oncogenes
Neoplasms
Carcinogenesis
Genome
Chronic Hepatitis B
Virus Diseases
Genes
Hepatocellular Carcinoma
Proteins
Liver

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Wild type HBx and truncated HBx : Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms. / Niller, Hans Helmut; Ay, Eva; Banati, Ferenc; Demcsák, Anett; Takács, M.; Mináróvits, J.

In: Reviews in Medical Virology, Vol. 26, No. 1, 01.01.2016, p. 57-73.

Research output: Contribution to journalArticle

@article{f7bb7fa640c5480abcb3bd118adc5ca9,
title = "Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms",
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.",
author = "Niller, {Hans Helmut} and Eva Ay and Ferenc Banati and Anett Demcs{\'a}k and M. Tak{\'a}cs and J. Min{\'a}r{\'o}vits",
year = "2016",
month = "1",
day = "1",
doi = "10.1002/rmv.1864",
language = "English",
volume = "26",
pages = "57--73",
journal = "Reviews in Medical Virology",
issn = "1052-9276",
publisher = "John Wiley and Sons Ltd",
number = "1",

}

TY - JOUR

T1 - Wild type HBx and truncated HBx

T2 - Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms

AU - Niller, Hans Helmut

AU - Ay, Eva

AU - Banati, Ferenc

AU - Demcsák, Anett

AU - Takács, M.

AU - Mináróvits, J.

PY - 2016/1/1

Y1 - 2016/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84954369590&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84954369590&partnerID=8YFLogxK

U2 - 10.1002/rmv.1864

DO - 10.1002/rmv.1864

M3 - Article

AN - SCOPUS:84954369590

VL - 26

SP - 57

EP - 73

JO - Reviews in Medical Virology

JF - Reviews in Medical Virology

SN - 1052-9276

IS - 1

ER -