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Homo sapiens strain:Mutu cell

ABSTRACT: Infection of Epstein-Barr virus in type III latency modulates biogenesis of exosomes and expression profile of exosomal miRNA in Burkitt lymphoma Mutu cell line

PROVIDER: PRJDB6853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR127190.fastq.gz	Fastqsanger.gz
	DRR127191.fastq.gz	Fastqsanger.gz
	DRR127192.fastq.gz	Fastqsanger.gz
	DRR127193.fastq.gz	Fastqsanger.gz
	DRR127194.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of MUTU I and MUTU III cells

Project description:RNAseq was used to identify host and viral transcriptome changes in MUTU I and MUTU III cells.

2020-05-04 | GSE136597 | GEO

Epstein-Barr virus growth/latency III program alters cellular microRNA expression

Project description:The Epstein-Barr virus (EBV) is associated with lymphoid and epithelial cancers. Initial EBV infection alters lymphocyte gene expression, inducing cellular proliferation and differentiation as the virus transitions through consecutive latency transcription programs. Cellular microRNAs (miRNAs) are important regulators of signaling pathways and are implicated in carcinogenesis. The extent to which EBV exploits cellular miRNAs is unknown. Using micro-array analysis and quantitative PCR, we demonstrate differential expression of cellular miRNAs in type III versus type I EBV latency including elevated expression of miR-21, miR-23a, miR-24, miR-27a, miR-34a, miR-146a and b, and miR-155. In contrast, miR-28 expression was found to be lower in type III latency. The EBV-mediated regulation of cellular miRNAs may contribute to EBV signaling and associated cancers. There were two major objectives for this study. The first objective was to determine whether EBV infected cells exhibiting type I latency influence cellular microRNA expression. For this study, four EBV negative derivatives of the type I latency cell line, Mutu I, were derived by retroviral infection with a dominant negative from of the EBV episomal replication factor, EBNA1. RNA from these four clones were compared to parental EBV positive Mutu I cells. Four dual labeling experiments were carried out for this comparison with dye reversal for every second pair of RNAs. The second objective was to determine whether EBV type III latency cells exhibit altered cellular microRNA gene expression compared to type I latency cells or EBV negative B cells. Four dual labeling experiments were carried out for this analysis with dye reversal for every second pair of RNAs.

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Transcriptome analysis of MUTU I and MUTU III cells

Project description:Transcriptome analysis of MUTU I and MUTU III cells

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The role of viral microRNAs in Burkitt Lymphoma: the Epstein Barr-encoded Bart-6-3p microRNA regulates cell proliferation and immunosurveillance

Project description:Compare Epstein-Barr-positive and Epstein-Barr-negative Burkitt lymphoma cases forboth cellular and viral microRNA expression profile, and to assess the role of viralmicroRNAs in Burkitt lymphomagenesis

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Homo sapiens strain:Mutu Cell Line, carrying Epstein-Barr virus

Project description:Homo sapiens strain:Mutu Cell Line, carrying Epstein-Barr virus Genome sequencing

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Expression data from Burkitt Lymphoma cell lines followed by expression or inhibition of ebv-BART6-3p microRNA

Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines.

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Identification of Host Biomarkers of EBV Latency IIb and Latency III

Project description:Deciphering the molecular pathogenesis of virally induced cancers is challenging due, in part, to the heterogeneity of both viral and host gene expression. Epstein-Barr Virus (EBV) is a ubiquitous herpesvirus prevalent in B-cell lymphomas of the immune suppressed. EBV infection of primary human B cells leads to their immortalization into lymphoblastoid cell lines (LCLs) serving as a model of these lymphomas. In previous studies, our lab has described a temporal model for immortalization with an initial phase characterized by expression of the Epstein-Barr Nuclear Antigens (EBNAs), high c-Myc activity, and hyper-proliferation in the absence of the Latent Membrane Proteins (LMPs), called latency IIb. This is followed by the long-term outgrowth of LCLs expressing the EBNAs along with the LMPs, particularly the NFkB-activating LMP1, defining latency III. LCLs, however, express a broad distribution of LMP1 such that a subset of these cells expresses LMP1 at levels seen in latency IIb, making it difficult to distinguish these two latency states. In this study, we performed mRNA-Seq on early EBV-infected latency IIb cells and latency III LCLs sorted by NFkB activity. We found that latency IIb transcriptomes clustered independently from latency III independent of NFkB. We identified and validated mRNAs defining these latency states. Indeed, we were able to distinguish latency IIb cells from LCLs expressing low levels of LMP1 using multiplex RNA-FISH targeting EBV EBNA2, LMP1, and human CCR7 or MGST1. This study defines latency IIb as a bona fide latency state independent from latency III and identifies biomarkers for understanding EBV-associated tumor heterogeneity

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Transcriptome analysis to UHRF1 depletion in MUTU I cells

Project description:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out MUTU I cells. UHRF1 KO MUTU I cells were subjected to FACSort for ICAM1+/GP350- and ICAM1-/GP350+ subpopulations, which were further used for RNAseq analysis. The MUTU I cells expressing control sgRNA was used as the control.

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Increased RNA Polymerase Activity at CTCF binding sites on the Epstein Barr Virus Genome During Reactivation from Latency

Project description:We used Precision Nuclear Run-on followed by Deep Sequencing (PRO-Seq) to investigate RNA Polymerase (Pol) activity during Epstein-Barr Virus (EBV) reactivation in EBV positive Burkitt's lymphoma cell lines Mutu-I and Akata. Nuclei were harvested from latent cells and after treatment with NaB/TPA (Mutu-I) or anti-IgG (akata) to stimulate reactivation at 1 and 4 and 12h. We identified multiple sites on the EBV genome enriched with Pol displaying distinct patterns of activity, which showed an association with CTCF and open chromatin.

2023-01-06 | GSE188584 | GEO

Homo sapiens

Project description:Epstein-Barr virus growth/latency III program alters cellular microRNA expression

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