Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of chromatin modifications in KSHV-transformed primary effusion lymphoma cell lines

ABSTRACT: Genome-wide maps of chromatin modifications in KSHV-transformed primary effusion lymphoma cell lines

PROVIDER: PRJNA559892 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9956030.fastq.gz	Fastqsanger.gz
	SRR9956031.fastq.gz	Fastqsanger.gz
	SRR9956032.fastq.gz	Fastqsanger.gz
	SRR9956023.fastq.gz	Fastqsanger.gz
	SRR9956033.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

Genome-wide maps of chromatin modifications in KSHV-transformed primary effusion lymphoma cell lines

Project description:The Kaposi's sarcoma-associated herpesviruses causes several cancers including Kaposi's sarcoma and primary effusion lymphoma (PEL). Our work reveals that the cellular transcription factors interferon regulatory factor 4 (IRF4) and basic leucine zipper ATF-like transcription factor (BATF), as well as the viral interferon regulatory factor 3 (vIRF3) are critical oncogenic dependencies specific to PEL cell lines. To understand the functions of these transcription factors, we performed ChIP-Seq on these proteins and other histone modifications in different PEL cell lines. Our results reveal that these oncogenic factors may cooperate to regulate the expression of the same mRNAs through promoter, enhancer, and superenhancer elements.

2020-08-13 | GSE135740 | GEO

RNA-seq analysis of KSHV-infected BCBL-1 cells, a primary effusion lymphoma cell line

Project description:Primari effusion lymphoma are (PEL) patient-derived transformed B-cells harboring latent Kaposi's sarcoma-associated herpesvirus (KSHV). The treatment of PEL cells with valproic acid (VA) leads to reactivation of KSHV and viral lytic replication. The aim of this project is to evaluate the effect of KSHV lytic infection on expression of the host transcriptome.

2021-11-08 | GSE179727 | GEO

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

Widespread traces of lytic KSHV in primary effusion lymphoma at single-cell resolution

Project description:Cancer cells of primary effusion lymphoma (PEL) often contain both Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). We measured the interplay of human, KSHV, and EBV transcription in a cell culture model of PEL using single-cell RNA sequencing. The data detect widespread trace expression of lytic KSHV genes.

2020-10-13 | GSE154900 | GEO

c-MET inhibitor inducing KSHV+ primary effusion lymphoma apoptosis

Project description:KSHV is a principal causative agent of primary effusion lymphoma (PEL). Despite this knowledge about the close relationship between HGF/c-MET network and solid tumors development, the role of HGF/c-MET in KSHV-related malignancies remains mostly unclear. We report that HGF/c-MET pathway is highly active within KSHV+ PEL cells and plays important role in tumor cell survival/growth. Targeting HGF/c-MET by a selective inhibitor, PF-2341066, significantly induces PEL apoptosis through a complex of underlying mechanisms, including cell-cycle arrest and DNA damage. By using microarray analysis, we have identified the global gene profile controlled by HGF/c-MET pathway within KSHV+ PEL cell-lines and several novel âdruggableâ candidates closely related to cancer cell survival/growth. Finally, we found that targeting HGF/c-MET pathway by PF-2341066 effectively prevents PEL tumor expansion and/or reduce established lymphoma progression in vivo. PEL cells were treated with vehicle control or c-MET inhibitor PF-2341066 (0.8 ÂµM) for 24 h, and the gene expression signature was compared to respective vehicle controls

2016-01-05 | E-GEOD-70594 | biostudies-arrayexpress

c-MET inhibitor inducing KSHV+ primary effusion lymphoma apoptosis

Project description:KSHV is a principal causative agent of primary effusion lymphoma (PEL). Despite this knowledge about the close relationship between HGF/c-MET network and solid tumors development, the role of HGF/c-MET in KSHV-related malignancies remains mostly unclear. We report that HGF/c-MET pathway is highly active within KSHV+ PEL cells and plays important role in tumor cell survival/growth. Targeting HGF/c-MET by a selective inhibitor, PF-2341066, significantly induces PEL apoptosis through a complex of underlying mechanisms, including cell-cycle arrest and DNA damage. By using microarray analysis, we have identified the global gene profile controlled by HGF/c-MET pathway within KSHV+ PEL cell-lines and several novel “druggable” candidates closely related to cancer cell survival/growth. Finally, we found that targeting HGF/c-MET pathway by PF-2341066 effectively prevents PEL tumor expansion and/or reduce established lymphoma progression in vivo.

2016-01-05 | GSE70594 | GEO

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

Genome-wide mapping of RTA binding sites in KSHV+ PEL cells during KSHV reactivation.

Project description:Chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) analysis was performed during Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation in KSHV+ recombinant primary effusion B-cell lymphoma cells (PEL). RTA binding sites were identified genome-wide in a recombinant PEL cell line called TRExBCBL1-3xFLAG-RTA cells at 12 hours post-induction (hpi) of RTA expression.

2019-01-09 | GSE123897 | GEO

Oncolytic reactivation of KSHV as a therapeutic approach for primary effusion lymphoma: high-resolution mapping of BRD4 binding sites in the KSHV genome

Project description:Primary effusion lymphoma (PEL) is an aggressive subtype of non-Hodgkin lymphoma caused by Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Currently, treatment options for patients with PEL are limited. Oncolytic viruses have been engineered as anticancer agents and have recently shown increased therapeutic promise. Similarly, lytic activation of endogenous viruses from latently infected tumor cells can also be applied as a cancer therapy. In theory, such a therapeutic strategy would induce oncolysis by viral replication, while simultaneously stimulating an immune response to viral lytic cycle antigens. We examined the combination of the FDA-approved drug ingenol-3-angelate (PEP005) with epigenetic drugs as a rational therapeutic approach for KSHV-mediated malignancies. JQ1, a bromodomain and extra terminal (BET) protein inhibitor, in combination with PEP005, not only robustly induced KSHV lytic replication, but also inhibited IL6 production from PEL cells. Using the dosages of these agents that was found to be effective in reactivating HIV (as a means to clear latent virus with highly active antiretroviral therapy), we were able to inhibit PEL growth in vitro and delay tumor growth in a PEL xenograft tumor model. KSHV reactivation was mediated by activation of NF-kB pathway by PEP005, which led to increased occupancy of RNA polymerase II onto the KSHV 33 genome. RNA-sequencing analysis further revealed cellular targets of PEP005, JQ1, and the synergistic effects of both. Thus, combination of PEP005 with a BET inhibitor may be considered as a rational therapeutic approach for the treatment of PEL.

2017-10-24 | GSE103395 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data