ArticleScientific reports2016
MicroRNA miR-204 and miR-1236 inhibit hepatitis B virus replication via two different mechanisms.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- An In-Depth Approach to the Associations between MicroRNAs and Viral Load in Patients with Chronic Hepatitis B-A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses.Respiratory research · 2020Pooled it
- Promising significance of the association of miR-204-5p expression with clinicopathological features of hepatocellular carcinoma.Medicine · 2017Pooled it
- In silico identification of microRNAs from the giant freshwater prawn Macrobrachium rosenbergii targeting white tail disease-associated viruses (MrNV and XSV).Virus genes · 2026Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Article
- Dysregulated microRNAs as a biomarker for diagnosis and prognosis of hepatitis B virus-associated hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- 3D engineered tissue models for studying human-specific infectious viral diseases.Bioactive materials · 2023Review
- LncRNA SNHG6 promotes G1/S-phase transition in hepatocellular carcinoma by impairing miR-204-5p-mediated inhibition of E2F1.Oncogene · 2021Article
- MicroRNA‑1271‑5p alleviates the malignant development of hepatitis B virus‑mediated liver cancer via binding to AQP5.Molecular medicine reports · 2021Article
- Advances in Multi-Omics Applications in HBV-Associated Hepatocellular Carcinoma.Frontiers in medicine · 2021Review
- Review
- Article
- Circulating miR-122 Is a Predictor for Virological Response in CHB Patients With High Viral Load Treated With Nucleos(t)ide Analogs.Frontiers in genetics · 2019Article
- Zika virus E protein alters the properties of human fetal neural stem cells by modulating microRNA circuitry.Cell death and differentiation · 2018Article
- Hepatitis B Virus Activates Signal Transducer and Activator of Transcription 3 Supporting Hepatocyte Survival and Virus Replication.Cellular and molecular gastroenterology and hepatology · 2017Article
- The role of microRNAs in hepatocyte metabolism and hepatitis B virus replication.Virologica Sinica · 2016Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) is a major human pathogen. In this study, we found that miR-204 and miR-1236 were down-regulated in HBV-producing cells, and each could suppress HBV replication. Using a bioinformatic approach and a reporter assay, we identified miR-1236, which can reduce HBV replication and protein production by directly targeting at HBV specific mRNA. In contrast, miR-204 was identified by a microarray approach, and had no effect on HBV RNA and protein production. Surprisingly, miR-204 could inhibit HBV pregenomic RNA encapsidation and capsid assembly. We further demonstrated that HBV suppressed miR-204 expression via activating a host transcription factor STAT3. We established a positive feed-forward loop between HBV, miR-204 and STAT3. Interestingly, miR-204 has been considered as a tumor suppressor in some literature. Since the risk for hepatocellular carcinoma (HCC) is significantly increased in chronic HBV patients, it is possible that chronic suppression of miR-204 by HBV contributes to HCC incidence. Both miR-204 and miR-1236 might be useful for developing new therapeutics against HBV.
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