Long noncoding RNA UCA1 regulates HCV replication and antiviral response via miR-145-5p/SOCS7/IFN pathway

Zeng, Haiyan; Li, Lei; Gao, Yi; Wu, Guojun; Hou, Zhouhua; Liu, Shuiping

doi:10.7150/ijbs.59227

Cited by 5 publications

(3 citation statements)

References 47 publications

(66 reference statements)

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“…BmN cells are susceptible to BmNPV infection and are commonly used to amplify the virus. Thus, it seems that BmSOCS7 may promote the replication of BmNPV, which is also consistent with previous findings that SOCS7 promotes the replication of HCV and HIV (Pan et al, 2019; Zeng et al, 2021). SOCS2 and SOCS6 from domesticated silkworms or Chinese oak silkworms can negatively regulate the production of AMPs to inhibit the antibacterial activity (Abbas et al, 2017; Abbas et al, 2021).…”

Section: Discussionsupporting

confidence: 91%

Cloning of suppressor of cytokine signaling 7 from silkworm (Bombyx mori) and its response to the infection of Bombyx mori nucleopolyhedrovirus

Wang,

Cui,

Zhang

et al. 2023

Arch Insect Biochem Physiol

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Suppressors of cytokine signaling (SOCS) play important roles in the regulation of growth, development, and immunity of eukaryotic organisms. SOCS7 is an important member of the SOCS family, but its physiological and pathological functions remain largely unknown in invertebrates including insects. Here, we first report the cloning of a SOCS7 gene from a domesticated silkworm (Bombyx mori), named BmSOCS7. We have characterized BmSOCS7 expression profiles in silkworm varieties susceptible or resistant to the infection of Bombyx mori nucleopolyhedrovirus (BmNPV) using the real‐time fluorescence quantitative PCR. BmSOCS7 expresses highly in embryogenesis and lowly in metamorphosis in resistant silkworms but does in opposite contrast in susceptible silkworms. Its expression is at very low level in the fat body of resistant silkworms but is relatively high in the fat body of susceptible ones. BmNPV inoculation induces a transient downregulation and then a general upregulation of BmSOCS7 expression in BmN cells, while it induces a general downregulation in silkworm midgut, fat body and hemolymph with more pronounced effect in resistant silkworms than susceptible ones and more prominent in the fat body and hemolymph than the midgut. Together, our work reveals that downregulation of BmSOCS7 expression may be an important strategy for silkworm anti‐BmNPV immune response, and BmSOCS7 may mainly function in the fat body and hemolymph rather than the midgut to participate in BmNPV infection process.

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Section: Discussionsupporting

confidence: 91%

Cloning of suppressor of cytokine signaling 7 from silkworm (Bombyx mori) and its response to the infection of Bombyx mori nucleopolyhedrovirus

Wang,

Cui,

Zhang

et al. 2023

Arch Insect Biochem Physiol

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“…Moreover, both miR-130b and miR-454 can inhibit Infectious Bursal Disease Virus (IBDV) replication by targeting host SOCS5 and SOCS6, respectively [76,77]. miR-145 targets SOCS7 and promotes interferon induction in bladder cancer cells [78] and Hepatitis C virus (HCV) [79]. In contrast, our study found that the bovine miR-193a-3p, miR-2375, and miR-12059 potentially bind to the host SOCS7 (Figure 7A,B), while SOCS1 only binds to miR-193a-3p.…”

Section: Impacts Of Host Mirna Targeting Various Bcov Genome Regions ...mentioning

confidence: 99%

The Potential Roles of Host Cell miRNAs in Fine-Tuning Bovine Coronavirus (BCoV) Molecular Pathogenesis, Tissue Tropism, and Immune Regulation

Shah,

Hemida

2024

Microorganisms

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Bovine coronavirus (BCoV) infection causes significant economic loss to the dairy and beef industries worldwide. BCoV exhibits dual tropism, infecting the respiratory and enteric tracts of cattle. The enteric BCoV isolates could also induce respiratory manifestations under certain circumstances. However, the mechanism of this dual tropism of BCoV infection has not yet been studied well. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and play a dual role in virus infection, mediating virus or modulating host immune regulatory genes through complex virus–host cell interactions. However, their role in BCoV infection remains unclear. This study aims to identify bovine miRNAs crucial for regulating virus–host interaction, influencing tissue tropism, and explore their potential as biomarkers and therapeutic agents against BCoV. We downloaded 18 full-length BCoV genomes (10 enteric and eight respiratory) from GenBank. We applied several bioinformatic tools to study the host miRNAs targeting various regions in the viral genome. We used the criteria of differential targeting between the enteric/respiratory isolates to identify some critical miRNAs as biological markers for BCoV infection. Using various online bioinformatic tools, we also searched for host miRNA target genes involved in BCoV infection, immune evasion, and regulation. Our results show that four bovine miRNAs (miR-2375, miR-193a-3p, miR-12059, and miR-494) potentially target the BCoV spike protein at multiple sites. These miRNAs also regulate the host immune suppressor pathways, which negatively impacts BCoV replication. Furthermore, we found that bta-(miR-2338, miR-6535, miR-2392, and miR-12054) also target the BCoV genome at certain regions but are involved in regulating host immune signal transduction pathways, i.e., type I interferon (IFN) and retinoic acid-inducible gene I (RIG-I) pathways. Moreover, both miR-2338 and miR-2392 also target host transcriptional factors RORA, YY1, and HLF, which are potential diagnostic markers for BCoV infection. Therefore, miR-2338, miR-6535, miR-2392, and miR-12054 have the potential to fine-tune BCoV tropism and immune evasion and enhance viral pathogenesis. Our results indicate that host miRNAs play essential roles in the BCoV tissue tropism, pathogenesis, and immune regulation. Four bovine miRNAs (miR-2375, bta-miR-193a-3p, bta-miR-12059, and bta-miR-494) target BCoV-S glycoprotein and are potentially involved in several immune suppression pathways during the viral infection. These miRNA candidates could serve as good genetic markers for BCoV infection. However, further studies are urgently needed to validate these identified miRNAs and their target genes in the context of BCoV infection and dual tropism and as genetic markers.

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“…LncRNA MALAT1 regulates Reactive Oxygen Species (ROS) and insulin production in male mice [ 20 ]. LncRNA UCA1 regulates antiviral response and HCV replication via the miR-145-5p/SOCS7/IFN axis [ 21 ]. HCV induces the downregulation of LncRNA Linc-Pint expression to evade the innate immune system [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis

Niu

Xia

et al. 2023

Analytical Cellular Pathology

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Background. Diabetes is one of the most common diseases and major public health burdens worldwide. Type 2 diabetes mellitus (T2DM) is associated with chronic hepatitis C virus (HCV) infection, and lncRNAs play an important role in HCV-induced T2DM. We aimed to explore the effect of lncRNA AC040162.3 on HCV-induced T2DM. Methods. HCV was used to infect MIN6 cells to establish an in vitro model. HCV copy number and miRNA expression were detected by Real Time Quantitative PCR (RT-qPCR). Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect the secretion of insulin, and methyl thiazolyl tetrazolium (MTT) was applied to analyze cell viability. Apoptosis was analyzed by Western blotting and flow cytometry. In addition, Western blotting and TdT-mediated dUTP Nick End Labeling (TUNEL) were used to analyze pyroptosis. Luciferase reporter assays were used to investigate the targeting relationship. Results. The expression of LncRNA AC040162.3 and NLRP3 was markedly increased in HCV–T2DM, while the expression of miR-223-3p was remarkably inhibited. In vitro experiments demonstrated that lncRNA AC040162.3 silencing or miR-223-3p overexpression remarkably alleviated HCV-induced T2DM deterioration by inhibiting cell apoptosis and pyroptosis and enhancing cell viability. We then demonstrated that silencing lncRNA AC040162.3 promoted the expression of miR-223-3p and that miR-223-3p bound to lncRNA AC040162.3 and the NLRP3 binding site. In addition, the protective effects of LncRNA AC040162.3 silencing in HCV-infected MIN6 cells were reversed by overexpression of NLRP3 or silencing of miR-223-3p. Conclusion. Silencing of lncRNA AC040162.3 alleviates the process of HCV-induced T2DM by governing the miR-223-3p/NLRP3 axis.

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Long noncoding RNA UCA1 regulates HCV replication and antiviral response via miR-145-5p/SOCS7/IFN pathway

Cited by 5 publications

References 47 publications

Cloning of suppressor of cytokine signaling 7 from silkworm (Bombyx mori) and its response to the infection of Bombyx mori nucleopolyhedrovirus

Cloning of suppressor of cytokine signaling 7 from silkworm (Bombyx mori) and its response to the infection of Bombyx mori nucleopolyhedrovirus

The Potential Roles of Host Cell miRNAs in Fine-Tuning Bovine Coronavirus (BCoV) Molecular Pathogenesis, Tissue Tropism, and Immune Regulation

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis

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