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MicroRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP

ABSTRACT: microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP

PROVIDER: PRJNA147457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR343332.fastq.gz	Fastqsanger.gz
	SRR343333.fastq.gz	Fastqsanger.gz
	SRR343334.fastq.gz	Fastqsanger.gz
	SRR343335.fastq.gz	Fastqsanger.gz
	SRR343336.fastq.gz	Fastqsanger.gz

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Similar Datasets

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP

Project description:This SuperSeries is composed of the following subset Series: GSE31745: Primary effusion lymphoma cell lines BC-1 and BC-3 GSE31746: BJAB Cell Lines Transduced with lentiviral vector pNL-SIN-CMV-AcGFP expressing KSHV miRNAs miR-K1, miR-K12-11, or miR-K4-3p GSE32109: microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina] Refer to individual Series

2011-11-16 | E-GEOD-32113 | biostudies-arrayexpress

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina]

Project description:Primary effusion lymphoma (PEL) is caused by Kaposi's sarcoma-associated herpesvirus (KSHV) and frequently also harbors Epstein-Barr virus (EBV). The expression of KSHV- and, often, EBV-encoded microRNAs (miRNAs) in PELs suggests a role for these miRNAs in viral latency and lymphomagenesis. Here we report the direct and transcriptome-wide identification of miRNA target sites for all miRNAs expressed in PEL cell lines. The resulting dataset revealed that KSHV miRNAs directly target more than 2000 cellular mRNAs encoding proteins that function in pathways with relevance to KSHV pathogenesis. Moreover, ~50% of these mRNAs are also targeted by EBV miRNAs, via distinct binding sites. In addition to a known viral analog of miR-155, we show that KSHV encodes a viral miRNA that mimics cellular miR-142-3p function. In summary, these experiments identify an extensive list of mRNAs targeted by KSHV miRNAs and indicate that these are likely to strongly influence viral replication and pathogenesis. small RNA sequencing, 3 samples Ago2 (EIF2C2) PAR-CLIP, 2 samples

2011-11-16 | E-GEOD-32109 | biostudies-arrayexpress

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina]

2011-11-16 | GSE32109 | GEO

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP

Project description:This SuperSeries is composed of the SubSeries listed below.

2011-11-16 | GSE32113 | GEO

Viral microRNA targetome of KSHV-infected primary effusion lymphoma cell lines.

Project description:Primary effusion lymphoma (PEL) is caused by Kaposi's sarcoma-associated herpesvirus (KSHV) and frequently also harbors Epstein-Barr virus (EBV). The expression of KSHV- and EBV-encoded microRNAs (miRNAs) in PELs suggests a role for these miRNAs in latency and lymphomagenesis. Using PAR-CLIP, a technology which allows the direct and transcriptome-wide identification of miRNA targets, we delineate the target sites for all viral and cellular miRNAs expressed in PEL cell lines. The resulting data set revealed that KSHV miRNAs directly target more than 2000 cellular mRNAs, including many involved in pathways relevant to KSHV pathogenesis. Moreover, 58% of these mRNAs are also targeted by EBV miRNAs, via distinct binding sites. In addition to a known viral analog of cellular miR-155, we show that KSHV encodes a viral miRNA that mimics cellular miR-142-3p function. In summary, this study identifies an extensive list of KSHV miRNA targets, which are likely to influence viral replication and pathogenesis.

| S-EPMC3222872 | biostudies-literature

Ago HITS-CLIP in KSHV-infected primary effusion lymphoma (PEL) cell lines BCBL-1 and BC-3

Project description:We performed Ago HITS-CLIP to identify targets of viral and human miRNAs in latently KSHV-infected PEL cells Ago HITS-CLIP was performed in two latently infected PEL cell lines, BCBL-1 and BC-3; Argonaute-immunoprecipitation of UV cross-linked Ago-miRNA-mRNA complexes, followed by RNA isolation, library construction, and high-throughput sequencing (Illumina GAxII); we performed 3 biological replicates for each cell line, two technical (sequencing) replicates of BCBL-1 biological replicate 1

2012-10-05 | E-GEOD-41357 | biostudies-arrayexpress

Mock or latently infected KSHV cells (BCBL, SLK and HFF)

Project description:[original title] Mock or latently infected KSHV cells (BCBL, SLK and HFF) vs common reference (mixture of RNA from both infected and uninfected cells). Expression profiling of latently infected cells using a custom tiling microarray. SLK and HFF cells were infected and selected for rKSHV.219. Mock infected SLK and HFF cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. Biological replicates were harvested and analyzed. Two condition experiment: mock infected vs. latently infected cells. Three cell types.

2010-06-05 | E-GEOD-20443 | biostudies-arrayexpress

Ago HITS-CLIP in KSHV-infected primary effusion lymphoma (PEL) cell lines BCBL-1 and BC-3

Project description:We performed Ago HITS-CLIP to identify targets of viral and human miRNAs in latently KSHV-infected PEL cells

2012-10-05 | GSE41357 | GEO

Mock or latently infected KSHV cells (BCBL, SLK and HFF)

2010-03-24 | GSE20443 | GEO

Oncolytic reactivation of KSHV as a therapeutic approach for primary effusion lymphoma: RNA-sequencing of PEL cell lines during KSHV reactivation

Project description:Primary effusion lymphoma (PEL) is an aggressive subtype of non-Hodgkin lymphoma caused by Kaposi’s sarcoma-associated herpesvirus infection, which is most commonly seen in HIV-positive patients. Induction of HIV reactivation by external stimuli in the presence of highly active anti-retroviral therapy (HAART) has been examined for its efficacy to eradicate latently infected HIV. Similary, lytic activation of viruses from latently infected tumor cells with anti-cancer drugs represents an effective strategy of anti-neoplastic therapy, through the induction of oncolysis by viral replication, stimulation of immune responses to the viral lytic antigens, and intrinsic effects of cancer drugs. Here we examined the combination of PEP005 with epigenetic drugs as a rational therapeutic strategy to target both in AIDS-associated KSHV-mediated malignancies. JQ1, a bromodomain and extra terminal protein (BET) inhibitor, in combination with a FDA-approved drug, PEP005, not only robustly induced KSHV lytic replication, but also inhibited IL-6 and VEGF production from PEL cells. This combination has been proposed for use in reactivation of HIV from latently infected T-cells, and the same combination and dosage inhibited PEL growth in vitro and delayed tumor growth in a PEL xenograft tumor model. Downstream activation of NF-B by PEP005 combined with sequestration of bromodomain-containing protein 4 (BRD4) by JQ1 robustly increased occupancy of RNA polymerase II onto the KSHV genome. RNA-sequencing analysis further revealed cellular targets of PEP005, JQ1, and the synergistic effects of both. We suggest that the combination of PEP005 with JQ1 should be considered as a rational therapeutic approach for HIV-associated PEL.

2017-11-03 | GSE89478 | GEO

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