Hepatitis B virus infection and alcohol consumption

Iida‐Ueno, Ayako; Enomoto, Masaru; Tamori, Akihiro; Kawada, Norifumi

doi:10.3748/wjg.v23.i15.2651

Cited by 62 publications

(53 citation statements)

References 61 publications

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“…HCC is the fifth most common malignant tumor and the second leading cause of cancer-related death worldwide [ 1 ]. HBV infection is the greatest risk factor for HCC [ 2 ]. Although enormous progress has been made in preventing HBV infection, diagnosis in the late stages of liver cancer and the highly metastatic nature of HCC are responsible for the high rate of HCC-related mortality.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: miR-3928v is induced by HBx via NF-κB/EGR1 and contributes to hepatocellular carcinoma malignancy by down-regulating VDAC3

Zhang

Song

Yao

et al. 2018

J Exp Clin Cancer Res

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BackgroundHepatitis B virus (HBV) plays a critical role in the tumorigenic behavior of human hepatocellular carcinoma (HCC). MicroRNAs (miRNAs) have been reported to participate in HCC development via the regulation of their target genes. However, HBV-modulated miRNAs involved in tumorigenesis remain to be identified. Here, we found that a novel highly expressed miRNA, TLRC-m0008_3p (miR-3928v), may be an important factor that promotes the malignancy of HBV-related HCC.MethodsSolexa sequencing was applied to profile miRNAs, and RT-qPCR was used to identify and quantitate miRNAs. We studied miR-3928v function in HCC cell lines by MTT, colony formation, migration/invasion, and vascular mimicry (VM) assays in vitro and by a xenograft tumor model in vivo. Finally, we predicted and verified the target gene of miR-3928v by a reporter assay, studied the function of this target gene, and cloned the promoter of miR-3928v and the transcription factor for use in dual-luciferase reporter assays and EMSAs.ResultsA variant of miR-3928 (miR-3928v) was identified and found to be highly expressed in HBV (+) HCC tissues. Voltage-dependent anion channel 3 (VDAC3) was validated as a target of miR-3928v and found to mediate the effects of miR-3928v in promoting HCC growth and migration/invasion. Furthermore, HBx protein increased early growth response 1 (EGR1) expression and facilitated its translocation into the nucleus to enhance miR-3928v promoter activity in an NF-κB signaling-dependent manner.ConclusionsmiR-3928v is induced by HBx through the NF-κB/EGR1 signaling pathway and down-regulates the tumor suppressor gene VDAC3 to accelerate the progression of HCC.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0681-y) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: miR-3928v is induced by HBx via NF-κB/EGR1 and contributes to hepatocellular carcinoma malignancy by down-regulating VDAC3

Zhang

Song

Yao

et al. 2018

J Exp Clin Cancer Res

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“…85,112 Histological evaluation also aids in the diagnosis and assessment of liver injury in comorbid conditions. [113][114][115][116][117] Prognostic utility of histology Ballooning, MDBs, lobular polymorphs, canalicular and/or ductular cholestasis, fibrosis and megamitochondria have been described as independent predictors of short-term outcome in patients with AH. In addition, visible bile in canaliculi and/or ductular reaction also predicted bacterial infection and sepsis.…”

Section: Histological Features and Diagnosis Of Ald Typesmentioning

confidence: 99%

EASL Clinical Practice Guidelines: Management of alcohol-related liver disease

Thursz¹,

Gual²,

Lackner³

et al. 2018

Journal of Hepatology

690

344

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The harmful use of alcohol has been estimated to cause approximately 3.3 million deaths every year, corresponding to nearly 6% of all deaths globally. Therefore, the effective management and treatment of alcoholic liver disease is a pertinent public health issue. In the following Clinical Practice Guidelines, the latest data on the treatment and management of alcohol-related liver disease will be reviewed and up to date recommendations for clinical management will be provided.

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“…A further interesting finding emerging from our conditional regression analysis is the independent contribution of alcohol abuse to liver cancer in HCV-infected subjects. There is ample evidence that alcohol synergistically contributes to the detrimental viral insult on liver disease progression [47,48]. HCV-infected patients are already discouraged from alcohol consumption: whether this needs to be reinforced in the presence of an unfavourable genetic profile, even after resolution of HCV infection, remains to be ascertained.…”

Section: Discussionmentioning

confidence: 99%

Interplay of PNPLA3 and HSD17B13 Variants in Modulating the Risk of Hepatocellular Carcinoma among Hepatitis C Patients

Benedittis

Bellan

Crevola

et al. 2020

Gastroenterology Research and Practice

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A single-nucleotide polymorphism causing a C to G change in the PNPLA3 gene (rs738409) is associated with disease severity and development of hepatocellular carcinoma (HCC) in nonalcoholic fatty liver disease; the insertion variant rs72613567:TA of the 17β-hydroxysteroid dehydrogenase type 13 (HSD17B13) mitigates this detrimental effect. Our aim was to evaluate if the same holds true in chronic hepatitis C virus infection (HCV). With a case control retrospective study design, we selected 110 patients who developed HCC on a background of HCV infection, matching each patient for sex and age (±30 months) to three HCV-infected, non-HCC patients. All participants underwent genotyping for PNPLA3 and HSD17B13 gene variants. Both univariate and multivariate analyses of risk factors for advanced disease and HCC were performed. Carriage of PNPLA3 G∗ allele was associated with a trend of progressively more severe liver disease, from mild fibrosis to significant fibrosis, cirrhosis, and HCC (p=0.007). When the HSD17B13:TA status of these patients was taken into account, the abovementioned trend was strengthened among HSD17B13 major allele homozygotes and completely blunted among carriers of the minor allele (p=0.0003 and 0.953, respectively). In a conditional logistic regression model including diabetes and AST to platelet ratio index among predictor variables, the unfavourable genetic profile characterized by the coexistence of the PNPLA3 minor allele and HSD17B13 major allele (vs. all other possible combinations) was an independent risk factor for HCC (OR=2.00, 95% CI: 1.23-3.26) together with a history of alcohol abuse. In conclusion, carriage of the combination PNPLA3 minor allele and HSD17B13 major allele may represent a risk factor for HCC among HCV-infected patients. The interplay between the two genes may explain some of the controversy on this topic and may be exploited to stratify HCC risk in hepatitis C.

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Hepatitis B virus infection and alcohol consumption

Cited by 62 publications

References 61 publications

RETRACTED ARTICLE: miR-3928v is induced by HBx via NF-κB/EGR1 and contributes to hepatocellular carcinoma malignancy by down-regulating VDAC3

RETRACTED ARTICLE: miR-3928v is induced by HBx via NF-κB/EGR1 and contributes to hepatocellular carcinoma malignancy by down-regulating VDAC3

EASL Clinical Practice Guidelines: Management of alcohol-related liver disease

Interplay of PNPLA3 and HSD17B13 Variants in Modulating the Risk of Hepatocellular Carcinoma among Hepatitis C Patients

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