The association of lncRNA SNPs and SNPs‐environment interactions based on GWAS with HBV‐related HCC risk and progression

Liu, Qing; Liu, Guiyan; Lin, Zhifeng; Lin, Ziqiang; Tian, Nana; Lin, Xinqi; Tan, Jianyi; Huang, Baoying; Ji, Xiaohui; Pi, Lucheng; Yu, Xiaofeng; Liu, Li; Gao, Yanhui

doi:10.1002/mgg3.1585

Cited by 7 publications

(3 citation statements)

References 32 publications

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“…LncRNA SNPs may play critical roles in HBV‐related HCC development. [ 34 ] In this regard, the current study explored the potential implication of certain genetic variations of one of the earliest identified lncRNAs; H19.…”

Section: Discussionmentioning

confidence: 99%

Association of long noncoding RNA H19 rs2839698 C/T with hepatitis B virus infection and hepatocellular carcinoma risk

Motawi,

Mady,

Elhelbawy

et al. 2024

J Biochem & Molecular Tox

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The intricate pathogenesis of the hepatitis B virus (HBV) and its progression to hepatocellular carcinoma (HCC) have not yet been fully elucidated. H19 is one of the earliest imprinted long noncoding RNAs (lncRNAs) associated with liver pathobiology. This study investigated the association of H19 single nucleotide polymorphisms (SNPs) rs2839698 C/T and rs217727 C/T with HBV and HBV‐related HCC and their correlation with H19 expression level. A total of 230 subjects were enrolled in this study including 100 HBV‐infected patients, 30 HBV‐related HCC patients, and 100 apparently healthy controls. TaqMan genotyping human assays were utilized to assess allelic discrimination for H19 SNPs. H19 expression was assessed using quantitative real‐time polymerase chain reaction (qRT‐PCR). Our findings showed that H19 rs2839698 was linked to a higher incidence of HBV infection and HBV‐related HCC. Individuals who bear the CT genotype of rs2839698 were more susceptible to HBV infection (OR = 3.05; 95% CI 1.714–5.457; p < 0.001). Those harboring the TT genotype were more prone to develop HCC (OR = 2.625; 95% CI 1.037–6.64; p = 0.038). Our data revealed that rs2839698 could function as a promising predictor of HCC risk. Furthermore, H19 was significantly downregulated in HBV (p < 0.01) and HCC (p < 0.01) patients versus the control group. Significant upregulation of H19 in HCC patients with cirrhosis (p < 0.001) was detected. Altogether, this is considered the first prospective case‐control study to address the implication of the genetic variations of H19 SNPs in HBV and HBV‐related HCC in Egyptian patients.

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Section: Discussionmentioning

confidence: 99%

Association of long noncoding RNA H19 rs2839698 C/T with hepatitis B virus infection and hepatocellular carcinoma risk

Motawi,

Mady,

Elhelbawy

et al. 2024

J Biochem & Molecular Tox

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“…The association of lnc-RP11-150O12.3 variants (rs2275959, rs1008547, and rs11776545) with HBV-related HCC risk and progression has been reported[ 107 ].…”

Section: Other Genetic Polymorphisms In Lncrnasmentioning

confidence: 99%

Long noncoding RNAs in hepatitis B virus replication and oncogenesis

Li¹,

Yang²,

Lo³

2022

WJG

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Several diverse long noncoding RNAs (lncRNAs) have been identified to be involved in hepatitis B virus (HBV) replication and oncogenesis, especially those dysregulated in HBV-related hepatocellular carcinoma (HCC). Most of these dysregulated lncRNAs are modulated by the HBV X protein. The regulatory mechanisms of some lncRNAs in HBV replication and oncogenesis have been characterized. Genetic polymorphisms of several lncRNAs affecting HBV replication or oncogenesis have also been studied. The prognosis of HCC remains poor. It is important to identify novel tumor markers for early diagnosis and find more therapeutic targets for effective treatments of HCC. Some dysregulated lncRNAs in HBV-related HCC may become biomarkers for early diagnosis and/or the therapeutic targets of HCC. This mini-review summarizes these findings briefly, focusing on recent developments.

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“…However, its molecular pathogenesis remains poorly understood. In the past two decades, there has been great progress in the identification of candidate HCC-related genetic and epigenetic risk or disease causal factors such as HLA - DRB , HLA-DQB1, and perhaps other HLA regions, PBX4 , PNPLA3 , GLUL, and STAT4 from genome-wide association studies (GWAS) [ 2 , 3 , 4 , 5 , 6 ]; genome-wide methylation differential analysis (GWMA) also have identified such examples as Ras association domain family member 1A ( RASSF1A ), P16, SLC22A20, PNPLA7 as epigenetic factors as well as their interaction [ 7 , 8 , 9 , 10 ]. However, the mechanism of how the virus, as the most important risk factor, interacts with genetic and epigenetics, is still not clear.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of DNA Methylation in Virus-Host Interaction in Hepatitis B Infection: Pathogenesis and Oncogenetic Properties

Zhang

Guo

Schrodi

2021

IJMS

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Hepatitis B virus (HBV), the well-studied oncovirus that contributes to the majority of hepatocellular carcinomas (HCC) worldwide, can cause a severe inflammatory microenvironment leading to genetic and epigenetic changes in hepatocyte clones. HBV replication contributes to the regulation of DNA methyltransferase gene expression, particularly by X protein (HBx), and subsequent methylation changes may lead to abnormal transcription activation of adjacent genes and genomic instability. Undoubtedly, the altered expression of these genes has been known to cause diverse aspects of infected hepatocytes, including apoptosis, proliferation, reactive oxygen species (ROS) accumulation, and immune responses. Additionally, pollutant-induced DNA methylation changes and aberrant methylation of imprinted genes in hepatocytes also complicate the process of tumorigenesis. Meanwhile, hepatocytes also contribute to epigenetic modification of the viral genome to affect HBV replication or viral protein production. Meanwhile, methylation levels of HBV integrants and surrounding host regions also play crucial roles in their ability to produce viral proteins in affected hepatocytes. Both host and viral changes can provide novel insights into tumorigenesis, individualized responses to therapeutic intervention, disease progress, and early diagnosis. As such, DNA methylation-mediated epigenetic silencing of cancer-related genes and viral replication is a compelling therapeutic goal to reduce morbidity and mortality from liver cancer caused by chronic HBV infection. In this review, we summarize the most recent research on aberrant DNA methylation associated with HBV infection, which is involved in HCC development, and provide an outlook on the future direction of the research.

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The association of lncRNA SNPs and SNPs‐environment interactions based on GWAS with HBV‐related HCC risk and progression

Cited by 7 publications

References 32 publications

Association of long noncoding RNA H19 rs2839698 C/T with hepatitis B virus infection and hepatocellular carcinoma risk

Association of long noncoding RNA H19 rs2839698 C/T with hepatitis B virus infection and hepatocellular carcinoma risk

Long noncoding RNAs in hepatitis B virus replication and oncogenesis

Mechanisms of DNA Methylation in Virus-Host Interaction in Hepatitis B Infection: Pathogenesis and Oncogenetic Properties

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