MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Wang, Ziqiang; Li, Kun; Wang, Xiaoxia; Huang, Weiren

doi:10.1080/15592294.2019.1600388

Cited by 25 publications

(17 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miR‐155 is abundantly expressed in dendritic cells, macrophages, active B cells, and T cells . In the present study, exogenous expression of miR‐155 in the brains of ICR suckling mice showed a protective effect against life‐threatening DENV infection (Figure 3).…”

Section: Discussionsupporting

confidence: 55%

MicroRNA‐155 inhibits dengue virus replication by inducing heme oxygenase‐1‐mediated antiviral interferon responses

Huang

et al. 2020

FASEB j.

View full text Add to dashboard Cite

MicroRNAs (miRNAs) have been reported to directly alter the virus life cycle and virus–host interactions, and so are considered promising molecules for controlling virus infection. In the present study, we observed that miR‐155 time‐dependently downregulated upon dengue virus (DENV) infection. In contrast, exogenous overexpression of miR‐155 appeared to limit viral replication in vitro, suggesting that the low levels of miR‐155 would be beneficial for DENV replication. In vivo, overexpression of miR‐155 protected ICR suckling mice from the life‐threatening effects of DENV infection and reduced virus propagation. Further investigation revealed that the anti‐DENV activity of miR‐155 was due to target Bach1, resulting in the induction of the heme oxygenase‐1 (HO‐1)‐mediated inhibition of DENV NS2B/NS3 protease activity, ultimately leading to induction of antiviral interferon responses, including interferon‐induced protein kinase R (PKR), 2′‐5′‐oligoadenylate synthetase 1 (OAS1), OAS2, and OAS3 expression, against DENV replication. Collectively, our results provide a promising new strategy to manage DENV infection by modulation of miR‐155 expression.

show abstract

Section: Discussionsupporting

confidence: 55%

MicroRNA‐155 inhibits dengue virus replication by inducing heme oxygenase‐1‐mediated antiviral interferon responses

Huang

et al. 2020

FASEB j.

View full text Add to dashboard Cite

show abstract

“…Hsa-miR-155-5p has been reported to modulate viral replication and viral gene expression in HSV-1 infections. 44 The functional analysis showed that these ceRNA network-related mRNAs were involved in regulating the immune system, T cell activation, the TNF signaling pathway, and the IL-17 signaling pathway. We speculated that lncRNA NEAT1 may also participate in regulating the immune response, cytokine storms or antiviral processes against SARS-CoV-2 by binding with key miRNAs, such as hsa-miR-100-5p and hsa-miR-155-5p.…”

Section: Discussionmentioning

confidence: 99%

Construction and Investigation of Competing Endogenous RNA Networks and Candidate Genes Involved in SARS-CoV-2 Infection

Qi¹,

Liu²,

Li³

et al. 2021

IJGM

View full text Add to dashboard Cite

Introduction:The current COVID-19 pandemic caused by a novel coronavirus SARS-CoV -2 is a quickly developing global health crisis, yet the mechanisms of pathogenesis in COVID-19 are not fully understood. Methods:The RNA sequencing data of SARS-CoV-2-infected cells was obtained from the Gene Expression Omnibus (GEO). The differentially expressed mRNAs (DEmRNAs), long non-coding RNAs (DElncRNAs), and microRNAs (DEmiRNAs) were identified by edgeR, and the SARS-CoV-2-associated competing endogenous RNA (ceRNA) network was constructed based on the prediction of bioinformatic databases. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted with the SARS-CoV-2-related DEmRNAs, and the protein-protein interaction network was also built basing on STRING database. The ROC analysis was performed for assessing the diagnostic efficiency of hub genes. Results:The results indicated that SARS-CoV-2-related DEmRNAs were associated with the interferon signaling pathway and other antiviral processes, such as IFNL3, IFNL1 and CH25H. Our analysis suggested that lncRNA NEAT1 might regulate the host immune response through two miRNAs, hsa-miR-374-5p and hsa-miR-155-5p, which control the expression of SOCS1, IL6, IL1B, CSF1R, CD274, TLR6, and TNF. Additionally, IFI6, HRASLS2, IGFBP4 and PTN may be potential targets based on an analysis comparing the transcriptional responses of SARS-CoV-2 infection with that of other respiratory viruses. Discussion: The unique ceRNA network identified potential non-coding RNAs and their possible targets as well as a new perspective to understand the molecular mechanisms of the host immune response to SARS-CoV-2. This study may also aid in the development of innovative diagnostic and therapeutic strategies.

show abstract

“…[23][24][25][26][27][28][29][30] Recently, it has been found that miR-155 can change the transcription initiation site of the serine/argininerich splicing factor 2 (SRSF2) promoter and regulate the protein kinase A (PKA) signaling pathway. 31 These findings suggest that miR-155 is directly or indirectly involved in epigenetic regulation.…”

Section: Introductionmentioning

confidence: 94%

miR-155 Accelerates the Growth of Human Liver Cancer Cells by Activating CDK2 via Targeting H3F3A

Xin

Xie

et al. 2020

Molecular Therapy - Oncolytics

View full text Add to dashboard Cite

miR-155 is associated with the promotion of tumorigenesis. Herein, we indicate that abnormal miR-155 was negatively correlated with the expression of P21WAF1/Cip1. Our results suggest that miR-155 alters the transcriptome and inhibits the expression of H3F3A in liver cancer cells. Therefore, miR-155 inhibits the methylation modification of histone H3 on the 27 th lysine. Notably, on the one hand, miR-155-dependent CTCF loops cause the CDK2 interacting with cyclin E in liver cancer cells; on the other hand, miR-155 promotes the phosphorylation modification of CDK2 by inhibiting H3F3A. Subsequently, miR-155 competitively blocks the binding of RNA polymerase II (RNA Pol II) to the P21WAF1/CIP1 promoter by increasing the phosphorylation of CDK2, inhibiting the transcription and translation of P21WAF1/CIP1. Strikingly, excessive P21WAF1/CIP1 abolishes the cancerous function of miR-155. In conclusion, miR-155 can play a positive role in the development of liver cancer and influence a series of gene expression through epigenetic regulation.

show abstract

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Cited by 25 publications

References 48 publications

MicroRNA‐155 inhibits dengue virus replication by inducing heme oxygenase‐1‐mediated antiviral interferon responses

MicroRNA‐155 inhibits dengue virus replication by inducing heme oxygenase‐1‐mediated antiviral interferon responses

Construction and Investigation of Competing Endogenous RNA Networks and Candidate Genes Involved in SARS-CoV-2 Infection

miR-155 Accelerates the Growth of Human Liver Cancer Cells by Activating CDK2 via Targeting H3F3A

Contact Info

Product

Resources

About