HBx protein of hepatitis B virus (HBV) can form complex with mitochondrial HSP60 and HSP70

Zhang, S. M.; Sun, Dejuan; Lou, Sai; Bo, Xiaochen; Lu, Zhi-Liang; Qian, Xuhong; Wang, S. Q.

doi:10.1007/s00705-005-0521-1

Cited by 46 publications

(44 citation statements)

References 19 publications

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“…It is also indicated that by causing the loss of mitochondrial membrane potential, HBx protein induces mitochondria-dependent apoptosis (Shirakata and Koike, 2003). Furthermore, HBx protein can form a complex with mitochondrial proteins, HSP60 and HSP70 that exerts effects on mitochondria-dependent apoptosis (Zhang et al, 2005a). HBx protein also may alter mitochondrial function by association with a member of the family of human mitochondrial voltage-dependent anion channel (HVDAC3) (Rahmani et al, 2000).…”

Section: Pro-apoptotic Effects Of Hbx Proteinmentioning

confidence: 99%

Hepatitis B virus-induced hepatocellular carcinoma: The role of the virus x protein

Motavaf¹,

Safari²,

Jourshari³

et al. 2013

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Summary. -Hepatocellular carcinoma (HCC) is one of the most common malignant diseases and has the fourth highest mortality rate worldwide. Chronic hepatitis B virus (HBV) infection has been identified as a major risk factor in HCC. Currently available evidence support a critical role of hepatitis B virus x (HBx) gene and protein in the pathogenesis of HBV-induced HCC. HBx protein is a multifunctional regulator that modulates cellular signal transduction pathways, transcriptional regulations, cell cycle progress, DNA repair, apoptosis, and genetic stability by interacting with different host factors. This review describes the current state of knowledge about the biological roles of this protein in the development of HCC. Abbreviations: DNMTs = DNA methyltransferases; HBV = hepatitis B virus; HBx = hepatitis B x protein; HCC = hepatocellular carcinoma; MMP = matrix metalloproteinase; MTA = metastasisassociated protein; RAR-β2 = retinoic acid receptor β2; TSGs = tumor suppressor genes; XPB = xeroderma pigmentosum B

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Section: Pro-apoptotic Effects Of Hbx Proteinmentioning

confidence: 99%

Hepatitis B virus-induced hepatocellular carcinoma: The role of the virus x protein

Motavaf¹,

Safari²,

Jourshari³

et al. 2013

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“…These interactions seem to alter the trans membrane potential and enhance HBx-mediated apoptosis. (38)(39)(40)(41) The biological role of HBx in HBV replication. X ORF is phylogenically conserved among mammalian hepadnavirus genomes, strongly indicating that HBx has some biological roles to facilitate or augment the viral life cycle.…”

Section: −10mentioning

confidence: 99%

Molecular functions and biological roles of hepatitis B virus x protein

Tang¹,

Oishi²,

Kaneko³

et al. 2006

Cancer Science

266

244

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Chronic infection of hepatitis B virus (HBV) isH epatitis B virus (HBV) infection is a worldwide health problem and is one of the major causes of hepatocellular carcinoma (HCC) in the world. However, new incidences of HBV infection have been dramatically reduced by several prevention programs. The crucial role of HBV in hepatocarcinogenesis is beyond doubt, however, the mechanism by which HBV causes transformation of hepatocytes remains uncertain.(1-3) Hepatitis B virus X protein (HBx) has long been suspected to play a positive role in hepatocarcinogenesis because HCC incidence has been reported in animals infected with mammalian hepadnaviruses. Among these hepadnaviruses, open reading frame-X (X-ORF) is conserved in the genomes. However, hepatocarcinogenesis has not been found in avian infected with avian hepadnaviruses where X-ORF is absent. In addition to the putative contribution of HBx, other oncogenic mechanisms of the HBV-related hepatocarcinogenesis have also been proposed, such as the integration-dependent scenario of HBV DNA in host genomes, (4) and the inflammation-dependent scenario.(5) Since no higher incidence of HCC has been reported in HBV-expressing transgenic mice, (6) host immunological responses to HBV infection (but not HBV proliferation by itself ) might be primarily contributing to the HBV-related hepatocarcinogenesis. HBx, a small protein of 154 amino acids, is a multifunctional regulator that modulates a variety of host processes through directly or indirectly interacting with virus and host factors. (2,3) In this short review, we briefly summarize the life cycle of HBV, expression of HBx, and the molecular functions of HBx. We then focus on the recent progress on the biological roles of HBx in HBV replication and cellular transformation. Expression and functions of HBx. HBV is a prototype of Hepadnaviridae, hepatotropic small DNA viruses, of which hosts are among limited species of water birds, squirrels and primates. The HBV genome is a 3.2-kb circular, partially double-stranded DNA molecule with four overlapping ORFs, PC-C, PS-S, P, and X-ORFs (Fig. 1). (7) Once HBV infection of hepatocytes occurs, its genome is converted to covalently closed circular (CCC) DNA, which serves as the template for transcription by the host RNA polymerase II, generating the 3.5-, 2.4-, 2.1-, and 0.7-kb transcripts under control of four HBV promoters (Cp, PS1p, Sp, and Xp), respectively (Fig. 1). Two HBV enhancers (Enh I and Enh II) positively regulate transcription of the HBV promoters in combination with the transcription factors that bind these promoters.(7-9) HBV replicates by reverse transcription of the viral pregenomic 3.5-kb RNA (pgRNA) using the HBV polymerase that catalyzes RNA-dependent DNA synthesis and DNA-dependent DNA synthesis. (7,10) The reverse transcription of hepadnaviruses is unique among DNA viruses, and the primer of the reverse transcription is a tyrosine residue of an N-terminal domain of Pol that is distinct from reverse transcription of retroviruses. (10)

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“…HBx exerts powerful effects on mitochondria either directly owing to their channel-forming activity or indirectly through interactions with endogenous channels (Takada et al, 1999;Henkler et al, 2001;Lee et al, 2004). HBx reportedly interacts with at least two mitochondrial proteins, namely heat-shock protein 60 and 70 (Tanaka et al, 2004;Zhang et al, 2005b) and the VDAC isoform VDAC3 (Rahmani et al, 2000;Kim, 2005).…”

Section: Hbxmentioning

confidence: 99%

Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis

et al. 2006

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As discussed in detail in other chapters of this review, chronic hepatitis B (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC). Most HCCs complicate the evolution of an active or inactive cirrhosis. However, some tumors occur on livers with minimal histological changes; the prevalence of such cases varies from one geographical region to the other, being much higher in the southern half of Africa (around 40% of HCCs) than in Asia, America and Europe, where at least 90% of HCCs are associated with the cirrhosis. This heterogeneity is probably a reflection of different environmental and genetic factors. This review will summarize the current knowledge on the mechanisms involved in HBVrelated liver carcinogenesis. It will show in particular how viruses can be viewed as tools to discover and dissect new cellular pathways involved in cancer development and emphasize the potential synergistic effects between HBV and hepatitis C virus, as well as between viral infections and other environmental factors, such as alcohol.

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HBx protein of hepatitis B virus (HBV) can form complex with mitochondrial HSP60 and HSP70

Cited by 46 publications

References 19 publications

Hepatitis B virus-induced hepatocellular carcinoma: The role of the virus x protein

Hepatitis B virus-induced hepatocellular carcinoma: The role of the virus x protein

Molecular functions and biological roles of hepatitis B virus x protein

Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis

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