ArticleThe Journal of international medical research2018
MicroRNA-520a suppresses HBV replication in HepG2.2.15 cells by inactivating AKT.
Article in The Journal of international medical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
4 citing papers in PubMed, 11 citations in OpenAlex.
- A Network Pharmacology Approach to Explore the Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- The Mechanisms of HBV-Induced Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021Review
- MiR-10a-5p-Mediated Syndecan 1 Suppression Restricts Porcine Hemagglutinating Encephalomyelitis Virus Replication.Frontiers in microbiology · 2020Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate whether the mechanism by which a microRNA, miR-520a, suppresses the replication of hepatitis B virus (HBV) involves the regulation of the serine/threonine kinase ( AKT) gene.
methodsThe effects of miR-520a on the proliferation, mitotic index and apoptosis of the HBV-replicating human hepatocellular carcinoma cell line HepG2.2.15 were measured using standard laboratory methods including flow cytometry. The effects of miR-520a on HBV transcription and replication were assessed using methods including immunoassays and reverse transcription-polymerase chain reaction. The effect of small interfering RNA (siRNA) to AKT on the levels of AKT mRNA and protein were also evaluated.
resultsIn HepG2.2.15 cells, miRNA-520a reduced HBV transcription and replication by reducing AKT levels. MiRNA-520a decreased cell proliferation and mitosis entry of cells and increased apoptosis in HepG2.2.15 cells. AKT levels were reduced significantly by its siRNA, which resulted in suppression of HBV replication in HepG2.2.15 cells.
conclusionsMiRNA-520a inhibited AKT gene expression and suppressed HBV transcription and replication. These findings suggest that miRNA-520a may be a novel target for the treatment of HBV infection because miRNA-520a reduced HepG2.2.15 cell survival and inhibited HBV replication associated with the AKT signalling pathway.
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Registered trials
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