Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CRISPR screens for synthetic rescue of cFLIP depletion in primary effusion lymphoma cell lines

ABSTRACT: Kaposi’s sarcoma-associated herpesvirus (KSHV) causes the B cell malignancy primary effusion lymphoma (PEL). We have previously shown that cultured PEL cell lines require expression of the cellular FLICE inhibitory protein (cFLIP) for survival (Manzano et al., Nat Comm 2018), although KSHV encodes a viral homolog of this protein (vFLIP). Here we employed genome-wide CRISPR/Cas9 synthetic rescue screens to identify loss of function perturbations that can compensate for cFLIP knockout/knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210445 | GEO | 2022/08/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

mRNA Sequencing of BC-1 Cells

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) causes the B cell malignancy primary effusion lymphoma (PEL). Here we performed mRNA sequencing to characterize the mRNA expression profile of the primary effusion lymhoma (PEL) cell line BC-1.

2022-08-10 | GSE210446 | GEO

A Computational Profiling of Changes in Gene Expression and Transcription Factors Induced by vFLIP K13 in Primary Effusion Lymphoma

Project description:Infection of Kaposi's sarcoma associated herpes virus (KSHV) has been linked to the development of primary effusion lymphoma (PEL), which is characterized by the loss of expression of B cell markers and effusions in the body cavities. This unique clinical feature of PEL has been attributed to their distinctive gene expression profile which shows overexpression of genes in various signaling pathways. KSHV-encoded latent protein vFLIP K13 has been shown to promote the survival and proliferation of PEL cells. In this study, we have employed gene array analysis followed by bioinformatics analysis of coordinated transcriptional factors network as well as biological pathways to characterize the effect of K13 on PEL-derived BCBL1 cells. We observed that genes associated with Cytokine signaling, Cell death, NF-kappaB and Cell adhesion pathways were differentially regulated by K13. We used computational approach complemented with microarrays to detail the global gene expression and identified distinct classes of differentially regulated genes in various cellular processes. We employed gene array analysis followed by bioinformatics analyses of coordinated transcriptional factors network as well as biological pathways to characterize the effect of K13 on in PEL-derived BCBL1 cells.

2012-05-20 | E-GEOD-37355 | biostudies-arrayexpress

Efficacy of bortezomib in a direct xenograft model of primary effusion lymphoma

Project description:Primary effusion lymphoma is an aggressive B-cell lymphoma most commonly diagnosed in HIV-positive patients and universally associated with Kaposi’s sarcoma-associated herpesvirus (KSHV). Chemotherapy treatment of PEL yields only short-term remissions in the vast majority of patients yet efforts to develop superior therapeutic approaches have been impeded by lack of animal models that more accurately mimic human disease. To address this issue we developed a direct xenograft model, UM-PEL-1, by transferring freshly-isolated human PEL cells into the peritoneal cavities of NOD/SCID mice without in vitro cell growth. We utilized this model to show that bortezomib induces PEL remission and extends overall survival of mice bearing lymphomatous effusions. Transcriptome analysis by genomic arrays revealed that bortezomib downregulated cell cycle progression, DNA replication, and Myc-target genes. The microarray analysis was conducted on mice bearing UM-PEL-1 xenografts after treatment for 24 hours with PBS or bortezomib. Both arms of the experiment had three mice and the RNA was pooled from the three treated mice for gene expression analysis.

2010-07-20 | E-GEOD-22594 | biostudies-arrayexpress

A Computational Profiling of Changes in Gene Expression and Transcription Factors Induced by vFLIP K13 in Primary Effusion Lymphoma

2012-05-21 | GSE37355 | GEO

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

Efficacy of bortezomib in a direct xenograft model of primary effusion lymphoma

2010-07-20 | GSE22594 | 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

Differentially expressed human and viral miRNAs across a panel of B-cell lines, including primary effusion lymphomas

Project description:To identify differentially expressed human and viral miRNAs across a panel of B-cell lines, including several primary effusion lymphomas (PEL). Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposi’s Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkitt’s lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression.

2015-12-05 | GSE18437 | GEO

Targeting ribonucleotide reductase by 3-AP in primary effusion lymphoma

Project description:KSHV is a principal causative agent of primary effusion lymphoma (PEL) which is lacking of effective treatment. Our previous data have showed that HGF/c-MET pathway is highly active within KSHV+ PEL cells and plays important role in tumor cell survival/growth. 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, including ribonucleotide reductase (RR). We continue to use microarray analysis to identify the gene profile affected within PEL cells exposure to RR inhibitor, 3-AP.

2018-01-01 | GSE91389 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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