The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Chen, Liyan; Ming, Xiaoyu; Li, Wensong; Bi, Man-Ru; Yan, Bin; Wang, Xiaoren; Yang, Pengfei; Yang, Baofeng

doi:10.1002/cbf.3488

Cited by 30 publications

(26 citation statements)

References 37 publications

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“…Various miRNAs can promote HBV replication via different mechanisms. [42][43][44][45] Our previous studies revealed that HBV could target RIG-I and RIG-G and inhibit STAT1 expression by inducing miR-146a expression, impairing the clearance of the virus via the innate immune system. 46,47 By analyzing the global miRNA expression profiles in HBV-associated HCC, it was found that the expression of many miRNAs, such as miR-150 and miR-342-3p, was altered.…”

Section: Hbv and Micrornamentioning

confidence: 99%

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

Yu¹,

Han²,

Zhao³

et al. 2021

JHC

137

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Hepatocellular carcinoma (HCC) is a common malignancy, and the hepatitis B virus (HBV) is its major pathogenic factor. Over the past decades, it has been confirmed that HBV infection could promote disease progression through a variety of mechanisms, ultimately leading to the malignant transformation of liver cells. Many factors have been identified in the pathogenesis of HBV-associated HCC (HBV-HCC), including HBV gene integration, genomic instability caused by mutation, and activation of cancer-promoting signaling pathways. As research in the progression of HBV-HCC progresses, the role of many new mechanisms, such as epigenetics, exosomes, autophagy, metabolic regulation, and immune suppression, is also being continuously explored. The occurrence of HBV-HCC is a complex process caused by interactions across multiple genes and multiple steps, where the synergistic effects of various cancer-promoting mechanisms accelerate the process of disease evolution from inflammation to tumorigenesis. In this review, we aim to provide a brief overview of the mechanisms involved in the occurrence and development of HBV-HCC, which may contribute to a better understanding of the role of HBV in the occurrence and development of HCC.

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Section: Hbv and Micrornamentioning

confidence: 99%

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

Yu¹,

Han²,

Zhao³

et al. 2021

JHC

137

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“…Socs1 is an important target gene of microrna-155 according to numerous previous studies (43,44). However, its functions in microvascular endothelial cells and VSMcs remain poorly studied.…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid inhibits vascular smooth muscle cell migration and proliferation by decreasing microRNA‑155 expression levels

Yin

et al. 2020

Mol Med Rep

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Vascular smooth muscle cell (VSMc) hyperplasia is a common cause of carotid restenosis. in the present study, the potential protective effects of docosahexaenoic acid (dHa) in carotid restenosis and the underlying mechanism of its effects were examined. VSMcs were treated with dHa, a polyunsaturated ω-3 fatty acid. cell migration and proliferation were assessed using wound healing and cell counting Kit-8 assays and by measuring Ki-67 protein levels. additionally, the expression levels of microrna-155 were determined by reverse transcription-quantitative Pcr (rT-qPcr). The involvement of microrna-155 in the regulation of migration and proliferation was evaluated by transfecting VSMcs with microrna mimics and inhibitors. Moreover, the reversal of migration and proliferation after transfection of VSMcs with the microrna mimics and subsequent treatment with dHa was investigated. A target gene of microRNA-155 was identified using RT-qPCR and luciferase assays. The migration and proliferation of VSMcs, as well as the expression of microrna-155 was inhibited by dHa stimulation. Microrna-155 regulated the migration and proliferation of VSMcs. Finally, proliferation and migration of VSMcs were reduced following dHa treatment, which was mediated by an increase in the expression levels of microrna-155. Suppressor of cytokine signalling 1 (Socs1) was the target gene of microrna-155. in conclusion, dHa inhibited VSMc migration and proliferation by reducing microrna-155 expression. This effect may be caused by the microrna-155 target gene Socs1.

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“…Induction of autophagy has been associated with many miRNAs including miR-146a-5p[ 178 ], the miR-99 family[ 179 ] and miR-192-3p, which is downregulated by HBx[ 180 ]. miR-155 has also been implicated in autophagy; however, this miRNA is downregulated following HBV infection[ 181 ]. HBV upregulates expression of miR-192-5p and miR-215-5p, which results in downregulation of apoptosis[ 182 ].…”

Section: Regulatory Noncoding Rnasmentioning

confidence: 99%

Silencing hepatitis B virus covalently closed circular DNA: The potential of an epigenetic therapy approach

Singh

Kairuz

Arbuthnot

et al. 2021

WJG

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Global prophylactic vaccination programmes have helped to curb new hepatitis B virus (HBV) infections. However, it is estimated that nearly 300 million people are chronically infected and have a high risk of developing hepatocellular carcinoma. As such, HBV remains a serious health priority and the development of novel curative therapeutics is urgently needed. Chronic HBV infection has been attributed to the persistence of the covalently closed circular DNA (cccDNA) which establishes itself as a minichromosome in the nucleus of hepatocytes. As the viral transcription intermediate, the cccDNA is responsible for producing new virions and perpetuating infection. HBV is dependent on various host factors for cccDNA formation and the minichromosome is amenable to epigenetic modifications. Two HBV proteins, X (HBx) and core (HBc) promote viral replication by modulating the cccDNA epigenome and regulating host cell responses. This includes viral and host gene expression, chromatin remodeling, DNA methylation, the antiviral immune response, apoptosis, and ubiquitination. Elimination of the cccDNA minichromosome would result in a sterilizing cure; however, this may be difficult to achieve. Epigenetic therapies could permanently silence the cccDNA minichromosome and promote a functional cure. This review explores the cccDNA epigenome, how host and viral factors influence transcription, and the recent epigenetic therapies and epigenome engineering approaches that have been described.

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The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Cited by 30 publications

References 37 publications

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

Docosahexaenoic acid inhibits vascular smooth muscle cell migration and proliferation by decreasing microRNA‑155 expression levels

Silencing hepatitis B virus covalently closed circular DNA: The potential of an epigenetic therapy approach

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