ArticleCell & bioscience2017
Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells.
Article in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
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- Roles of Non-Coding RNAs in Virus-Host Interaction About Pathogenesis of Hand-Foot-Mouth Disease.Current microbiology · 2022Review
- MicroRNA let-7 and viral infections: focus on mechanisms of action.Cellular & molecular biology letters · 2022Review
- MicroRNAs based regulation of cytokine regulating immune expressed genes and their transcription factors in COVID-19.Meta gene · 2022Article
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
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- Essential Role of Non-Coding RNAs in Enterovirus Infection: From Basic Mechanisms to Clinical Prospects.International journal of molecular sciences · 2021Review
- Dual Effects of Let-7b in the Early Stage of Hepatitis C Virus Infection.Journal of virology · 2021Article
- Host MicroRNA hsa-miR-494-3p Promotes EV71 Replication by Directly Targeting PTEN.Frontiers in cellular and infection microbiology · 2018Article
- Random walks on mutual microRNA-target gene interaction network improve the prediction of disease-associated microRNAs.BMC bioinformatics · 2017Article
- Kv1.3 channel blocker (ImKTx88) maintains blood-brain barrier in experimental autoimmune encephalomyelitis.Cell & bioscience · 2017Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman enterovirus 71 (EV71) causes severe hand, foot and mouse disease, accompanied by neurological complications. During the interaction between EV71 and the host, the virus subverts host cell machinery for its own replication. However, the roles of microRNAs (miRNAs) in this process remain obscure.
resultsIn this study, we found that the miRNA hsa-let-7c-5p was significantly upregulated in EV71-infected rhabdomyosarcoma cells. The overexpression of hsa-let-7c-5p promoted replication of the virus, and the hsa-let-7c-5p inhibitor suppressed viral replication. Furthermore, hsa-let-7c-5p targeted mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) and inhibited its expression. Interestingly, downregulation of MAP4K4 expression led to an increase in EV71 replication. In addition, MAP4K4 knockdown or transfection with the hsa-let-7c-5p mimic led to activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway, whereas the hsa-let-7c-5p inhibitor inhibited activation of this pathway. Moreover, EV71 infection promoted JNK pathway activation to facilitate viral replication.
conclusionsOur data suggested that hsa-let-7c-5p facilitated EV71 replication by inhibiting MAP4K4 expression, which might be related to subversion of the JNK pathway by the virus. These results may shed light on a novel mechanism underlying the defense of EV71 against cellular responses. In addition, these findings may facilitate the development of new antiviral strategies for use in future therapies.
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