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Wild-type versus HBx-transfected mive

ABSTRACT: Hepatitis B virus (HBV) has been clearly recognized as an etiological factor for hepatocellular carcinoma (HCC). HBV encodes the potentially oncogenic HBx protein. We aimed to elucidate the molecular mechanism of HCC caused by HBx and to discover the biomarker related to HCC by HBx. Three experimental groups, 3, 9 and 13 month aged HBx Tg mice and age matched normal wild type B6 mouse which have same background of HBx Tg mice were used to find differentially expressed genes during HCC. Keywords: Genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE12723 | GEO | 2008/09/11

SECONDARY ACCESSION(S): PRJNA112663

REPOSITORIES: GEO

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Wild-type versus HBx-transfected mive

Project description:Hepatitis B virus (HBV) has been clearly recognized as an etiological factor for hepatocellular carcinoma (HCC). HBV encodes the potentially oncogenic HBx protein. We aimed to elucidate the molecular mechanism of HCC caused by HBx and to discover the biomarker related to HCC by HBx. Three experimental groups, 3, 9 and 13 month aged HBx Tg mice and age matched normal wild type B6 mouse which have same background of HBx Tg mice were used to find differentially expressed genes during HCC. Keywords: Genetic modification 3-month-old, 9-month-old, 13-month-old wild type B6 mice vs 3-month-old, 9-month-old, 13-month-old HBx transfected mice; Biological replicates at each timepoint; 9 controls vs 9 HBx-mice

2010-06-19 | E-GEOD-12723 | biostudies-arrayexpress

DNA methylation analysis of normal and HBx transgenic mouse liver

Project description:A genome-wide integrated DNA methylation analysis of the early stage of hepatocellular carcinoma development that induced by HBx. The HBV x (HBx) protein, which plays a critical role in the development of HCC, was shown to interact with several epigenetic factors, such as DNMT3A and HDAC1. Most HBx transgenic (TG) mice spontaneously develop HCC at about 1 year of age, providing genetic validation of the oncogenic potential of HBx even in the absence of viral integration and chronic inflammation. Therefore, it would be intriguing to study the regulatory role of HBx in the epigenome and its impact on HCC development. We performed a genome-wide analysis to examine the differences in DNA methylation enrichment pattern between cancer and normal liver cells.

2019-01-21 | GSE77059 | GEO

ChIP-seq analysis of normal and HBx transgenic mouse liver

Project description:A genome-wide integrated ChIP-seq analysis of the early stage of hepatocellular carcinoma development that induced by HBx. The HBV x (HBx) protein, which plays a critical role in the development of HCC, was shown to interact with several epigenetic factors, such as DNMT3A and HDAC1. Most HBx transgenic (TG) mice spontaneously develop HCC at about 1 year of age, providing genetic validation of the oncogenic potential of HBx even in the absence of viral integration and chronic inflammation. Therefore, it would be intriguing to study the regulatory role of HBx in the epigenome and its impact on HCC development. We performed a genome-wide analysis to examine the differences in histone modification and RNA pol II enrichment pattern between cancer and normal liver cells.

2019-01-20 | GSE77023 | GEO

DNA methylome and transcriptome analysis of normal and HBx transgenic mouse liver

Project description:A genome-wide integrated methylome and transcriptome analysis of the early stage of hepatocellular carcinoma development that induced by HBx. The HBV x (HBx) protein, which plays a critical role in the development of HCC, was shown to interact with several epigenetic factors, such as DNMT3A and HDAC1. Most HBx transgenic (TG) mice spontaneously develop HCC at about 1 year of age, providing genetic validation of the oncogenic potential of HBx even in the absence of viral integration and chronic inflammation. Therefore, it would be intriguing to study the regulatory role of HBx in the epigenome and its impact on HCC development. We performed a genome-wide analysis to examine the differences in DNA methylation patterns and RNA transcriptions between cancer and normal liver cells. High-throughput sequencing analysis of MIRA (methylated CpG island recovery assay) and mRNA at 3 mouth old age mouse liver

2013-06-19 | E-GEOD-48052 | biostudies-arrayexpress

DNA methylome and transcriptome analysis of normal and HBx transgenic mouse liver

2013-06-19 | GSE48052 | GEO

Identification of substrates of the CRL4-HBx E3 ubiquitin ligase

Project description:Hepatitis B Virus (HBV) remains a major public health problem, and is a major cause liver cancer worldwide. HBV infection in vivo requires the function of the HBx protein, which facilitates expression of viral genes from the episomal genome by an unknown mechanism. Evidence suggests that HBx functions as a targeting subunit for the CRL4 E3 ubiquitin ligase, redirecting the complex to target and degrade an unknown host restriction factor. We used substrate trapping proteomics to search for ubiquitylation substrates of HBx. We used MLN4924 to block CRL activity and stabilize interactions between HBx and its substrates. We then performed APMS to identify bound proteins and potential substrates.

2016-09-29 | PXD004762 | Pride

Episomal HBV persistence within transcribed host nuclear chromatin compartments involves HBx

Project description:In hepatocyte nuclei, hepatitis B virus (HBV) genomes occur episomally as covalently closed circular DNA (cccDNA). The HBV X protein (HBx) is required to initiate and maintain HBV replication and acts as host gene trans-regulator. However, functionally relevant spatiotemporal localization and interactions of cccDNA and HBx remain to be understood. This is the first study utilizing circularized chromosome conformation capture (4C) to identify regional virus-host genome interactions. We combined 4C with RNA-seq and ChIP-seq to illuminate the nuclear landscape associated with HBV episomes and HBx. Moreover, we functionally studied HBx-binding to episomal HBV DNA. In human HBV-positive HepaRG hepatocytes, 4C and ChIP revealed specific nuclear localization of HBV episomes and HBx associated with actively transcribed nuclear domains correlating well in size with constrained topological units built up by chromatin fibre loops, which are believed to constitute fundamental cell nuclear architectural units. Interestingly, HBx alone occupied transcribed chromatin domains, and its binding to HBV episomes depended on its C-terminus in vitro. In conclusion, HBx and HBV DNA similarly follow higher-order nuclear assembly patterns, specifically favoring transcriptionally active nuclear compartments. These novel observations may shed light on important unsolved problems: to understand the long-term episomal stability and the facilitation of viral persistence.

2018-04-30 | GSE100400 | GEO

Hepatitis B virus X protein contributes to hepatocellular carcinoma via upregulation of KIAA1429 methyltransferase and mRNA m6A hypermethylation of HSPG2/Perlecan [MeRIP-Seq]

Project description:Chronic hepatitis B virus (HBV) remains to be the most common risk factor of hepatocellular carcinoma (HCC). While work has primarily focussed on understanding the direct and indirect mechanisms of Hepatitis B virus X protein (HBx) mediated hepatocarcinogenesis, from genetic and epigenetic perspectives, its influence on RNA modification mediated onset of liver malignancies is less well understood. This study explored the role of HBV-encoded HBx in altering the m6A methylome profile and its implications on the pathogenesis of HCC. We established HBx expressing stable HCC cell lines, Huh7-HBx and HepG2-HBx, and explored the transcriptomic and epitranscriptomic profiles by RNA-seq and MeRIP-seq, respectively. Preliminary results suggest that HBx promotes liver cell proliferation, migration, survival and overall m6A methylation in HCC cells and is involved in modulating the extracellular matrix. We show that HBx mediates liver cell transformation by upregulating KIAA1429 methyltransferase. HBx also drives the expression and hypermethylation of the extracellular matrix protein HSPG2/Perlecan and promotes tumourigenesis. Our findings indicate a potential interaction between KIAA1429 and HSPG2, thus could be novel targets in combating HBx-driven HCC and warrants further investigation.

2023-08-09 | GSE240450 | GEO

Hepatitis B virus X protein contributes to hepatocellular carcinoma via upregulation of KIAA1429 methyltransferase and mRNA m6A hypermethylation of HSPG2/Perlecan [RNA-Seq]

2023-08-09 | GSE240394 | GEO

Huh-7 exosomes and HBV - Quantitative Proteomic Analysis of Exosome Protein Content Changes Induced by Hepatitis B Virus in Huh-7 Cells Using SILAC Labeling and LC-MS/MS

Project description:Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this project, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS.

2014-10-09 | PXD001339 | Pride

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