MiR-29c inhibits HCV replication<i>via</i>activation of type I IFN response by targeting STAT3 in JFH-1-infected Huh7 cells

Wang, Yanjing; Li, Yuanyuan

doi:10.1039/c7ra12815k

Cited by 7 publications

(6 citation statements)

References 27 publications

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“…The result suggested that STAT3 is involved in the development of cholesteatoma, and it was indicative of the high proliferation of the cholesteatoma epithelium. Meanwhile, various studies have shown that STAT3 is epigenetically regulated by miRNAs [ 34 , 35 ]. The results of statistical analysis of correlation showed that miR-125b and STAT3 were negatively correlated in cholesteatoma ( Figure 1 E ).…”

Section: Discussionmentioning

confidence: 99%

Low expression of microRNA-125b enhances the expression of STAT3 and contributes to cholesteatoma growth

et al. 2019

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Introduction: MicroRNA-125b has been found to be down-regulated in many types of malignant tumours and diseases with excessive proliferation of keratinocytes, such as cutaneous squamous cell carcinoma and psoriasis. Cholesteatoma, which is mainly composed of keratinocytes, also has characteristics of abnormal proliferation similar to a malignant tumour. However, the expression and regulatory mechanisms of miR-125b and its downstream genes in cholesteatoma have not been clarified. Material and methods: Real time fluorescence quantitative PCR was applied to detect the expression of miR-125b in the cholesteatoma and corresponding retroauricular skin. Immunohistochemical staining and western blot were used to detect signal transducers and activators of transcription 3 (STAT3) and the downstream gene cyclinD1, survivin, and vascular endothelial growth factor (VEGF) in the cholesteatoma and corresponding retroauricular skin. The targeted regulatory relationship between miR-125b and STAT3 was confirmed by dual luciferase reporter assay. Proliferation and apoptosis of transfected HaCaT cells were detected by MTS, cell cycle, and apoptosis assays. Results: We observed down-regulation of miR-125b and up-regulation of STAT3, cyclinD1, survivin, and VEGF in cholesteatoma tissues. STAT3 was a direct target gene of miR-125b. Inhibition of miR-125b enhanced STAT3 and its downstream genes expression, promoted HaCaT cell proliferation, and inhibited apoptosis. Conclusions: The results of this study demonstrate that miR-125b can influence the growth of cholesteatoma by targeting STAT3 and its downstream genes, including cyclinD1, survivin, and VEGF, thus providing an opportunity to establish new medical therapy strategies and facilitating further study of the pathogenesis of cholesteatoma.

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Section: Discussionmentioning

confidence: 99%

Low expression of microRNA-125b enhances the expression of STAT3 and contributes to cholesteatoma growth

et al. 2019

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“…However, in patients with HIV/HCV co-infection, a down-regulation of serum levels of miR-29a was shown when compared to healthy control group and patients with HIV infection [ 59 ]. In vitro, HCV decreases the expression of miR-29 activating HSCs and miR-29c has been shown to repress HCV replication targeting STAT3 and induce the production of IFN I [ 96 , 97 ].…”

Section: Mirnas Expression During Chb and Chc Related Fibrosismentioning

confidence: 99%

miRNAs as Potential Biomarkers for Viral Hepatitis B and C

Loureiro

Tout

Narguet

et al. 2020

Viruses

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Around 257 million people are living with hepatitis B virus (HBV) chronic infection and 71 million with hepatitis C virus (HCV) chronic infection. Both HBV and HCV infections can lead to liver complications such as cirrhosis and hepatocellular carcinoma (HCC). To take care of these chronically infected patients, one strategy is to diagnose the early stage of fibrosis in order to treat them as soon as possible to decrease the risk of HCC development. microRNAs (or miRNAs) are small non-coding RNAs which regulate many cellular processes in metazoans. Their expressions were frequently modulated by up- or down-regulation during fibrosis progression. In the serum of patients with HBV chronic infection (CHB), miR-122 and miR-185 expressions are increased, while miR-29, -143, -21 and miR-223 expressions are decreased during fibrosis progression. In the serum of patients with HCV chronic infection (CHC), miR-143 and miR-223 expressions are increased, while miR-122 expression is decreased during fibrosis progression. This review aims to summarize current knowledge of principal miRNAs modulation involved in fibrosis progression during chronic hepatitis B/C infections. Furthermore, we also discuss the potential use of miRNAs as non-invasive biomarkers to diagnose fibrosis with the intention of prioritizing patients with advanced fibrosis for treatment and surveillance.

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“…It has been found that miR-221 was able to enhance IFNα's anti-HCV effect through SOCS1 and SOCS3 targeting [74]. miR-29c appeared to be protective against HCV infection by its effect on enhancing the STAT3-mediated type I IFN response in Huh7 cells [75]. miR-29 suppresses the immune response to intracellular bacterial infection by targeting IFN-γ [76].…”

Section: Discussionmentioning

confidence: 99%

Analysis of lncRNA, miRNA, and mRNA Expression Profiling in Type I IFN and Type II IFN Overexpressed in Porcine Alveolar Macrophages

Han

et al. 2021

International Journal of Genomics

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Current data is scarce regarding the function of noncoding RNAs (ncRNAs) such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in the interferon- (IFN-) mediated immune response. This is a comprehensive study that analyzes the lncRNA and miRNA expression profiles of the type I IFN and type II IFN in porcine alveolar macrophages using RNA sequencing. There was a total of 152 overexpressed differentially expressed (DE) lncRNAs and 21 DE miRNAs across type I IFN and type II IFN in porcine alveolar macrophages. Subsequent lncRNA-miRNA-mRNA network construction revealed the involvement of 36 DE lncRNAs and 12 DE miRNAs. LncRNAs such as the XLOC_211306, XLOC_100516, XLOC_00695, XLOC_149196, and XLOC_014459 were expressed at a higher degree in the type I IFN group, while XLOC_222640, XLOC_047290, XLOC_147777, XLOC_162298, XLOC_220210, and XLOC_165237 were expressed at a higher degree in the type II IFN group. These lncRNAs were found to act as “sponges” for miRNAs such as miR-34a, miR-328, miR-885-3p, miR-149, miR-30c-3p, miR-30b-5p, miR-708-5p, miR-193a-5p, miR-365-5p, and miR-7. Their target genes FADS2, RPS6KA1, PIM1, and NOD1 were found to be associated with several immune-related signaling pathways including the NOD-like receptor, Jak-STAT, mTOR, and PPAR signaling pathways. These experiments provide a comprehensive profile of overexpressed noncoding RNAs in porcine alveolar macrophages, providing new insights regarding the IFN-mediated immune response.

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MiR-29c inhibits HCV replicationviaactivation of type I IFN response by targeting STAT3 in JFH-1-infected Huh7 cells

Abstract: MiR-29c, a member of the miR-29 family, has been recognized to play an important role in hepatitis C virus (HCV) infection.

Cited by 7 publications

References 27 publications

Low expression of microRNA-125b enhances the expression of STAT3 and contributes to cholesteatoma growth

Low expression of microRNA-125b enhances the expression of STAT3 and contributes to cholesteatoma growth

miRNAs as Potential Biomarkers for Viral Hepatitis B and C

Analysis of lncRNA, miRNA, and mRNA Expression Profiling in Type I IFN and Type II IFN Overexpressed in Porcine Alveolar Macrophages

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