ArticleHepatology (Baltimore, Md.)2019
Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR-192-3p-XIAP Through NF kappa B Signaling.
Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- Interplay between Cellular Autophagy and Hepatitis B Virus Replication: A Systematic Review.Cells · 2020Pooled it
- Virus-host interactome reveals host cellular pathways perturbed by tick-borne encephalitis virus infection.iScience · 2026Article
- Mechanistic insight into complement C3 regulation during chronic HBV infection: effect on viral persistence and host immune response.Journal of biomedical science · 2026Article
- Protein quality control and antigen presentation in the development of hepatitis B-related hepatocellular carcinoma.Frontiers in pharmacology · 2026Review
- Mitochondrial respiratory chain regulates HBV clearance through dual modulation of lysosomal acidification.Emerging microbes & infections · 2025Article
- Interferon-induced miR-7705 modulates the anti-virus activity of cholesterol 25-hydroxylase.Journal of virology · 2025Article
- HBV promotes epithelial-mesenchymal transition in HCC and liver fibrosis through JNK-mediated autophagy.Hepatology communications · 2025Article
- miR-215 Modulates Ubiquitination to Impair Inflammasome Activation and Autophagy DuringAnimals : an open access journal from MDPI · 2025Article
- Unveiling the impact of non-coding RNAs on virus-induced cellular autophagy: roles and research advances.Frontiers in microbiology · 2025Review
- Dual-specificity tyrosine-regulated kinase 4 modulates the STAT3-FOS signaling axis to inhibit hepatitis B virus replicationInternational journal of biological sciences · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- MicroRNAs in Hepatocellular Carcinoma Pathogenesis: Insights into Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Understanding lactate in the development of Hepatitis B virus-related hepatocellular carcinoma.Infectious agents and cancer · 2024Review
- The Potential Role of Autophagy in Progression of Liver Fibrosis in Chronic Hepatitis B Patients Receiving Antiviral Treatment: A Brief Report.Iranian journal of medical sciences · 2024Article
- Mechanism study of oleanolic acid derivative, K73-03, inducing cell apoptosis in hepatocellular carcinoma.Cancer cell international · 2024Article
- mTOR Signaling: Roles in Hepatitis B Virus Infection and Hepatocellular Carcinoma.International journal of biological sciences · 2024Review
- Hepatitis B virus promotes its own replication by enhancing RAB5A-mediated dual activation of endosomal and autophagic vesicle pathways.Emerging microbes & infections · 2023Article
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Exosomal MicroRNA and Protein Profiles of Hepatitis B Virus-Related Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Hepatitis B virus (HBV) is a major risk factor for the development and progression of hepatocellular carcinoma. It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Here, we report that decreasing levels of the expression of the miRNA miR-192-3p is associated with rising levels of HBV DNA in the serum of HBV patients. We revealed that HBV infection repressed the expression of miR-192-3p through hepatitis B x protein interaction with c-myc. We further showed that miR-192-3p was repressed by HBV transfection in vitro and in a mouse model, leading to cellular autophagy. Using an miRNA target prediction database miRBase, we identified X-linked inhibitor of apoptosis protein (XIAP) as a target gene of miR-192-3p and demonstrated that miR-192-3p directly targeted the XIAP 3'-untranslated region of XIAP messenger RNA. Importantly, we discovered that HBV promoted autophagy through miR-192-3p-XIAP axis and that this process was important for HBV replication in vitro and in vivo. We demonstrated that miR-192-3p functioned through the nuclear factor kappa B signaling pathway to inhibit autophagy, thereby reducing HBV replication. Conclusions: Our findings indicate that miR-192-3p is a regulator of HBV infection and may play a potential role in hepatocellular carcinoma. It may also serve as a biomarker or therapeutic target for HBV patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.