HBV precore G1896A mutation promotes growth of hepatocellular carcinoma cells by activating ERK/MAPK pathway

Zhao, Bin; Qiao, Hai; Zhao, Yan; Gao, Zhiyun; Wang, Weijie; Yan, Chen; Li, Jian; Guo, Zhanjun; Xia, Chen; Chiu, Sandra

doi:10.1016/j.virs.2023.06.004

Cited by 3 publications

(2 citation statements)

References 51 publications

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“…The G1896A stop codon mutation in the preC region results in HBeAg translation stopping prematurely ( Mohebbi et al, 2012 ; Tsuge, 2021 ). A recent study showed that G1896A mutation could promote HCC tumor growth in vivo by enhancing HBV replication and activating of ERK/MAPK pathway ( Zhao et al, 2023 ). Also, a natural double mutation in the basal core promoter (BCP), A1762T/G1764A (TA), has been suggested as a risk factor for HCC ( Yang et al, 2016 ).…”

Section: Hbv Mutations and Impacts On Hccmentioning

confidence: 99%

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

Shoraka,

Hosseinian,

Hasibi

et al. 2023

Front. Microbiol.

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Hepatocellular carcinoma (HCC) is a significant global health issue, with a high prevalence in many regions. There are variations in the etiology of HCC in different regions, but most cases are due to long-term infection with viral hepatitis. Hepatitis B virus (HBV) is responsible for more than 50% of virus-related HCC, which highlights the importance of HBV in pathogenesis of the disease. The development and progression of HBV-related HCC is a complex multistep process that can involve host, viral, and environmental factors. Several studies have suggested that some HBV genome mutations as well as HBV proteins can dysregulate cell signaling pathways involved in the development of HCC. Furthermore, it seems that the pathogenicity, progression of liver diseases, response to treatment and also viral replication are different among HBV mutants. Understanding the relationship between HBV genome variations and host signaling pathway alteration will improve our understanding of the molecular pathogenesis of HBV-related HCC. Furthermore, investigating commonly dysregulated pathways in HBV-related HCC is necessary to discover more specific therapeutic targets and develop more effective strategies for HCC treatment. The objective of this review is to address the role of HBV in the HCC progression and primarily focus on the impacts of HBV genome variations on HCC-related signaling pathways.

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Section: Hbv Mutations and Impacts On Hccmentioning

confidence: 99%

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

Shoraka,

Hosseinian,

Hasibi

et al. 2023

Front. Microbiol.

View full text Add to dashboard Cite

show abstract

“…Explosive studies have been focused on the role of G1896A mutation in viral replication since the first report in late 1980s. However, conflicting results still exist in either clinical studies ( Lau et al., 2021 ; Nakashima et al., 2004 ; Pivert et al., 2015 ; Ouneissa et al., 2012 ) or in vitro experiments ( Samal et al., 2015 ; Koumbi et al., 2016 ; Zhao et al., 2023 ). In addition, A1762T/G1764A, the double mutations located in the basal core promoter (BCP) region, have also attracted great concern.…”

Section: Introductionmentioning

confidence: 99%

Precore mutation enhances viral replication to facilitate persistent infection especially in HBeAg-negative patients

Li,

Yang,

Liu

et al. 2024

Virologica Sinica

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Evolution and diversity of the hepatitis B virus genome: Clinical implications

Xie,

2024

Virology

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HBV precore G1896A mutation promotes growth of hepatocellular carcinoma cells by activating ERK/MAPK pathway

Cited by 3 publications

References 51 publications

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways

Precore mutation enhances viral replication to facilitate persistent infection especially in HBeAg-negative patients

Evolution and diversity of the hepatitis B virus genome: Clinical implications

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