Role of microRNAs in hepatitis B virus replication and pathogenesis

Liu, Wan–Hsin; Yeh, Shiou–Hwei; Chen, Pei‐Jer

doi:10.1016/j.bbagrm.2011.04.008

Cited by 75 publications

(75 citation statements)

References 89 publications

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“…Using TargetScan (29), we confirmed multiple microRNAs that have been characterized previously to target specific sites in HBV transcripts (14). In these analyses, we additionally identified three sites in the coding region for HBp and one in the overlapping region between HBp and HBx that could be targeted by miR-15a and miR-16-1 ( Fig.…”

Section: Resultssupporting

confidence: 55%

“…For instance, while most microRNAs characterized to date inhibit viral replication by targeting specific HBV transcripts, miR-1 has been shown to enhance HBV replication by targeting the host gene HDAC4 (14). To determine the net effect of the microRNA machinery on HBV replication, we knocked down the key component of the RISC complex Ago2 in hepatocytes (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Hepatitis B Viral RNA Directly Mediates Down-regulation of the Tumor Suppressor MicroRNA miR-15a/miR-16-1 in Hepatocytes

Wang

Jiang

Xiong

et al. 2013

Journal of Biological Chemistry

101

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Background: Hepatitis B virus (HBV) infection has been linked to the development of hepatocellular carcinoma (HCC) in humans. Results: Specific microRNAs inhibit HBV replication, and HBV infection also reprograms microRNA expression. Conclusion:The viral HBx RNA directly mediates the down-regulation of the tumor suppressor microRNA miR-15a/miR-16-1. Significance: The functional interplay between HBV infection and microRNA may contribute to HCC development.

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Section: Resultssupporting

confidence: 55%

Section: Resultsmentioning

confidence: 99%

Hepatitis B Viral RNA Directly Mediates Down-regulation of the Tumor Suppressor MicroRNA miR-15a/miR-16-1 in Hepatocytes

Wang

Jiang

Xiong

et al. 2013

Journal of Biological Chemistry

101

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“…miR-122 is a highly abundant liver-specific miRNA and is frequently downregulated in liver cancers. It functions as a tumor suppressor by directly targeting several positive regulators of cell cycle progression that have been implicated in tumorigenesis, including SRF, Igf1R, ADAM 17, ADAM10, cyclin G1, Wnt1, Bcl-w and PI3CG [47][48][49][50][51]. As a proto-oncogene, cyclin G1 is closely related to cancer [52].…”

Section: Deregulated Mirnas Involved In the Cell Cyclementioning

confidence: 99%

miRNAs affect the development of hepatocellular carcinoma via dysregulation of their biogenesis and expression

Chu

Duan

et al. 2014

Cell Communication and Signaling

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The pathogenesis of hepatocellular carcinoma (HCC) is not fully understood, which has affected the early diagnosis and treatment of HCC and the survival time of patients. MicroRNAs (miRNAs) are a class of evolutionarily conserved small, non-coding RNAs, which regulate the expression of various genes post-transcriptionally. Emerging evidence indicates that the key enzymes involved in the miRNA biosynthesis pathway and some tumor-specific miRNAs are widely deregulated or upregulated in HCC and closely associated with the occurrence and development of various cancers, including HCC. Early studies have shown that miRNAs have critical roles in HCC progression by targeting many critical protein-coding genes, thereby contributing to the promotion of cell proliferation; the avoidance of apoptosis, inducing via angiogenesis; and the activation of invasion and metastasis pathways. Experimental data indicate that discovery of increasing numbers of aberrantly expressed miRNAs has opened up a new field for investigating the molecular mechanism of HCC progression. In this review, we describe the current knowledge about the roles and validated targets of miRNAs in the above pathways that are known to be hallmarks of HCC, and we also describe the influence of genetic variations in miRNA biosynthesis and genes.

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“…MicroRNA (miRNA) is known to play an important regulatory role in differentiation, development, and infectious diseases (Ambros 2011). Many HCC-related microRNAs have been reported (Liu et al 2011;Szabo and Bala 2013); however, the roles of microRNAs in liver physiology and pathology have remained to be explored.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

Huang

Chou

Lee

et al. 2015

RNA

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In hepatitis B virus (HBV)-replicating hepatocytes, miR-130a expression was significantly reduced. In a reciprocal manner, miR130a reduced HBV replication by targeting at two major metabolic regulators PGC1α and PPARγ, both of which can potently stimulate HBV replication. We proposed a positive feed-forward loop between HBV, miR-130a, PPARγ, and PGC1α. Accordingly, HBV can significantly enhance viral replication by reducing miR-130a and increasing PGC1α and PPARγ. NF-κB/ p65 can strongly stimulate miR-130a promoter, while miR-130a can promote NF-κB/p65 protein level by reducing PPARγ and thus NF-κB/p65 protein degradation. We postulated another positive feed-forward loop between miR-130a and NF-κB/p65 via PPARγ. During liver inflammation, NF-κB signaling could contribute to viral clearance via its positive effect on miR-130a transcription. Conversely, in asymptomatic HBV carriers, persistent viral infection could reduce miR-130a and NF-κB expression, leading to dampened inflammation and immune tolerance. Finally, miR-130a could contribute to metabolic homeostasis by dual targeting PGC1α and PPARγ simultaneously.

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Role of microRNAs in hepatitis B virus replication and pathogenesis

Cited by 75 publications

References 89 publications

Hepatitis B Viral RNA Directly Mediates Down-regulation of the Tumor Suppressor MicroRNA miR-15a/miR-16-1 in Hepatocytes

Hepatitis B Viral RNA Directly Mediates Down-regulation of the Tumor Suppressor MicroRNA miR-15a/miR-16-1 in Hepatocytes

miRNAs affect the development of hepatocellular carcinoma via dysregulation of their biogenesis and expression

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

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