MicroRNA-155 Is an Epstein-Barr Virus-Induced Gene That Modulates Epstein-Barr Virus-Regulated Gene Expression Pathways

Yin, Qinyan; McBride, Jane; Fewell, Claire; Lacey, Michelle; Wang, Xia; Lin, Zhen; Cameron, Jennifer E.; Flemington, Erik K.

doi:10.1128/jvi.02380-07

Cited by 237 publications

(243 citation statements)

References 50 publications

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“…The expression profile of ZNF652 in these cell lines resembles an inverse reflection of their miR-155 expression profiles, which is consistent with previous reports demonstrating that miR-155 targets the ZNF652 transcript through a specific seed sequence in the 3'UTR (19,20). Indeed, over-expression of miR-155 markedly reduced endogenous ZNF652 protein levels in the H1299 epithelial lung carcinoma cell line ( Figure 4C …”

Section: Znf652 Is An Epithelial Marker and Suppresses Tumor Cell Invsupporting

confidence: 90%

Mutant p53 drives invasion in breast tumors through up-regulation of miR-155

et al. 2012

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When a manuscript is accepted for publication in an NPG journal, authors are encouraged to submit the author's version of the accepted paper (the unedited manuscript) to PubMedCentral or other appropriate funding body's archive, for public release six months after publication. In addition, authors are encouraged to archive this version of the manuscript in their institution's repositories and, if they wish, on their personal websites, also six months after the original publication.

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Section: Znf652 Is An Epithelial Marker and Suppresses Tumor Cell Invsupporting

confidence: 90%

Mutant p53 drives invasion in breast tumors through up-regulation of miR-155

et al. 2012

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“…miR-155 is also induced by LPS, as well as other TLR ligands and pro-inflammatory cytokines (10). Numerous targets have been identified for miR-155 such as c-Maf, Bach1, PU.1, C/ebp␤, and SHIP1; however, their role in TLR signaling has never been extensively explored before (12)(13)(14)(15)(16)(17). Mice deficient in miR-155 have defects in B cell differentiation, as well as possessing severe deficiencies in immune responses when exposed to pathogens, thus highlighting the important role miR-155 plays in the immune system as a whole (12,18,19).…”

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confidence: 99%

IL-10 Inhibits miR-155 Induction by Toll-like Receptors

McCoy

Sheedy

Qualls

et al. 2010

Journal of Biological Chemistry

234

180

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IL-10 is a potent anti-inflammatory cytokine that is crucial for down-regulating pro-inflammatory genes, which are induced by Toll-like receptor (TLR) signaling. In this study, we have examined whether modulation of microRNAs plays a role in the inhibitory effect of IL-10 on TLR4 signaling. Analyzing microRNAs known to be induced by TLR4, we found that IL-10 could inhibit the expression of miR-155 in response to lipopolysaccharide but had no effect on miR-21 or miR-146a. IL-10 inhibited miR-155 transcription from the BIC gene in a STAT3-dependent manner. This inhibitory effect of IL-10 on miR-155 led to an increase in the expression of the miR-155 target, SHIP1. This is the first example of IL-10 playing a role in microRNA function and suggests that through its inhibitory effect on miR-155, IL-10 has the ability to promote anti-inflammatory gene expression.

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“…Additionally, the increased level of miRNA-155 was demonstrated in EpsteinBarr virus (EBV)-infected lymphocytes displaying type III latency. In this study, an elevation of miR-155 was found to be responsible for the alteration of EBV gene expression profile (21). Our study is the first report showing that the higher expression level of miRNA-155 is associated with the HCV RNA replication in PBMCs.…”

Section: Discussionmentioning

confidence: 50%

“…Blood samples were collected from 47 untreated, chronic hepatitis C patients (34 males, 13 females: ages [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] to identify the presence of HCV RNA in serum and genomic/ antigenomic HCV RNA strands in PBMCs. The study was accepted by the Bioethical Committee of the Medical University of Lodz (RNN/93/07/kB); blood samples were collected after informed consent had been obtained.…”

Section: Methodsmentioning

confidence: 99%

Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells

Sidorkiewicz¹

2011

Int J Mol Med

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Abstract.A tight relationship has been revealed between cellular microRNAs (miRNAs) and the course of hepatitis C virus (HCV) replication in human hepatoma cells. Although the detection of the antigenomic HCV RNA strand in peripheral blood mononuclear cells (PBMCs) has provided evidence for viral replication in PBMCs, no reports have shown how miRNAs are affected upon HCV RNA synthesis in PBMCs. The aim of the present study was to assess if and how the expression levels of miRNA-155 and miRNA-196b in PBMCs are related to HCV replication in PBMCs of chronic hepatitis C (CHC) patients. Supporting analyses were performed to evaluate the expression of precursor pri-miR-155 (BIC) and Dicer protein.The genomic and antigenomic HCV RNA strands in PBMCs were detected by strand-specific qRT-PCR. The expression levels of miRNAs, BIC RNA and Dicer protein were assayed on PBMCs by qRT-PCR and Western blotting, respectively. miRNA-155 and miRNA-196b were detected in all studied PBMC samples, but their levels varied according to the presence of the antigenomic HCV RNA strand in PBMCs. Increased expression levels of miRNA-155 and miRNA-196b were associated with the presence of the antigenomic HCV RNA strand in PBMCs. In this group of patients higher frequency of BIC RNA and Dicer protein detection was also found. This study demonstrates that HCV RNA replication in PBMCs of CHC patients is connected with the increased and coordinated expression of miRNA-155 and miRNA-196b.

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MicroRNA-155 Is an Epstein-Barr Virus-Induced Gene That Modulates Epstein-Barr Virus-Regulated Gene Expression Pathways

Abstract: The cellular microRNA miR-155 has been shown to be involved in lymphocyte activation and is expressed in

Cited by 237 publications

References 50 publications

Mutant p53 drives invasion in breast tumors through up-regulation of miR-155

Mutant p53 drives invasion in breast tumors through up-regulation of miR-155

IL-10 Inhibits miR-155 Induction by Toll-like Receptors

Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells

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