Epstein-Barr Virus-Encoded Latent Membrane Protein 1 (LMP1) Induces the Expression of the Cellular MicroRNA miR-146a

Motsch, Natalie; Pfuhl, Thorsten; Mrázek, Jan; Barth, Stephanie; Grässer, Friedrich A.

doi:10.4161/rna.4.3.5206

Cited by 179 publications

(158 citation statements)

References 36 publications

Supporting

Mentioning

141

Contrasting

Unclassified

Order By: Relevance

“…miR-29a/b/c and miR-146a are among those miRs that are highly induced by LMP1. Previous findings that LMP1 induces miR-146a are consistent with our results (Motsch et al, 2007;Cameron et al, 2008). Supplementary Figure 1 shows the heat map of the miR profile.…”

Section: Mir Profiling Of U2932 Dlbcls Transfected With Lmp1supporting

confidence: 91%

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

et al. 2009

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) is noted for its transforming potential. Yet, it also acts as a cytostatic and growth-relenting factor in Burkitt's lymphoma (BL) cells. The underlying molecular mechanisms of the growth inhibitory property of LMP1 have remained largely unknown. In this study, we show that LMP1 negatively regulates a major oncogene, TCL1, in diffuse large B-cell lymphoma (DLBCL) and BL cells. MicroRNA (miR) profiling of LMP1 transfectants showed that among others, miR-29b, is upregulated. LMP1 diminished TCL1 by inducing miR29b through C-terminus activation region 1 (CTAR1) and CTAR2. miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. The miR-29b increase by LMP1 was due to an increase in the cluster pri-miR-29b1-a transcription, derived from human chromosome 7. Using pharmacological inhibitors, we found that p38 mitogen-activated protein kinase-activating function of LMP1 is important for this effect. The ability of LMP1 to negatively regulate TCL1 through miR-29b might underlie its B-cell lymphoma growth antagonistic property. As LMP1 is also important for B-cell transformation, we suggest that the functional dichotomy of this viral protein may depend on a combination of levels of its expression, lineage and differentiation of the target cells and regulation of miRs, which then directs the outcome of the cellular response.

show abstract

Section: Mir Profiling Of U2932 Dlbcls Transfected With Lmp1supporting

confidence: 91%

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Similarly to miRNA-146a, miRNA-155 has also been implicated in a variety of pathologies 8,9,10 . However, in the case of SS and in relation to the viral differentially expressed microRNA reported in this article, the relation of miRNA-155 to Epstein-Barr virus infection (EBV) 11,12 and the association of this microRNA to lymphomas deserve further evaluation 13,14,15 .…”

Section: Human and Viral Microrna Expression In Sjögren Syndromementioning

confidence: 99%

Human and Viral microRNA Expression in Sjögren Syndrome

Cotrim

Alevizos

2014

J Rheumatol

View full text Add to dashboard Cite

“…Northern blotting analysis was carried out as described (18,19). The membranes were analyzed with a PhosphoImager (Amersham-Biosciences).…”

Section: Northern Blottingmentioning

confidence: 99%

The MicroRNA Profile of Prostate Carcinoma Obtained by Deep Sequencing

Szczyrba

Löprich²,

Wach³

et al. 2010

Molecular Cancer Research

Self Cite

207

View full text Add to dashboard Cite

Prostate cancer is a leading cause of tumor mortality. To characterize the underlying molecular mechanisms, we have compared the microRNA (miRNA) profile of primary prostate cancers and noncancer prostate tissues using deep sequencing. MiRNAs are small noncoding RNAs of 21 to 25 nucleotides that regulate gene expression through the inhibition of protein synthesis. We find that 33 miRNAs were upregulated or downregulated >1.5-fold. The deregulation of selected miRNAs was confirmed by both Northern blotting and quantitative reverse transcription-PCR in established prostate cancer cell lines and clinical tissue samples. A computational search indicated the 3′-untranslated region (UTR) of the mRNA for myosin VI (MYO6) as a potential target for both miR-143 and miR-145, the expression of which was reduced in the tumor tissues. Upregulation of myosin VI in prostate cancer was previously shown by immunohistochemistry. The level of MYO6 mRNA was significantly induced in all primary tumor tissues compared with the nontumor tissue from the same patient. This finding was matched to the upregulation of myosin VI in established prostate cancer cell lines. In luciferase reporter analysis, we find a significant negative regulatory effect on the MYO6 3′UTR by both miR-143 and miR-145. Mutation of the potential binding sites for miR-143 and miR-145 in the MYO6 3′ UTR resulted in a loss of responsiveness to the corresponding miRNA. Our data indicate that miR-143 and miR-145 are involved in the regulation of MYO6 expression and possibly in the development of prostate cancer. Mol Cancer Res; 8(4); 529-38. ©2010 AACR.

show abstract

Epstein-Barr Virus-Encoded Latent Membrane Protein 1 (LMP1) Induces the Expression of the Cellular MicroRNA miR-146a

Cited by 179 publications

References 36 publications

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

Human and Viral microRNA Expression in Sjögren Syndrome

The MicroRNA Profile of Prostate Carcinoma Obtained by Deep Sequencing

Contact Info

Product

Resources

About