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Transcriptomic analysis of gene profile in KSHV+ PEL cells changed by bacterial quorum sensing molecules [BCBL_OdDHL]

ABSTRACT: KSHV-related primary effusion lymphoma is mostly seen in immunocompromised individuals such as HIV+ patients, who frequently suffering polymicrobial infections including different opportunistic pathogens. It is interesting to explore the host gene profile in PEL altered by bacterial quorum sensing molecules, the key systems regulating virulence factors in many bacteria.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110172 | GEO | 2018/05/22

REPOSITORIES: GEO

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Transcriptomic analysis of gene profile in KSHV+ PEL cells changed by bacterial quorum sensing molecules [BCP-1_OdDHL]

Project description:KSHV-related primary effusion lymphoma is mostly seen in immunocompromised individuals such as HIV+ patients, who frequently suffering polymicrobial infections including different opportunistic pathogens. It is interesting to explore the host gene profile in PEL altered by bacterial quorum sensing molecules, the key systems regulating virulence factors in many bacteria.

2018-05-22 | GSE110173 | GEO

Transcriptomic analysis of gene profile in KSHV+ PEL cells changed by bacterial quorum sensing molecules [BCP-1]

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Transcriptomic analysis of gene profile in KSHV+ PEL cells changed by bacterial quorum sensing molecules [BCBL-1]

2018-05-22 | GSE110074 | 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

Global host gene expression changes in KSHV+ PEL cells upon KSHV reactivation

Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) is a human oncogenic virus, which maintains the persistent infection of the host by intermittently reactivating from latently infected cells to produce viral progenies. Here, we performed a comprehensive time course transcriptome analysis during KSHV reactivation in KSHV+ primary effusion B-cell lymphoma cells (PEL). For this we used a recombinant PEL cell line called TRExBCBL1-3xFLAG-RTA. The expression of the N-terminally 3xFLAG-tagged RTA was induced by adding 1 μg/ml doxycycline (Dox) to the medium. Total gene expression changes were identified in TRExBCBL1-3xFLAG-RTA cells at 0, 6, 12, and 24 hours post-induction (hpi).

2019-01-09 | GSE123898 | GEO

Altered global gene profile in KSHV+ PEL cells exposure to dhC16-Cer

Project description:Primary effusion lymphoma (PEL) is a rare B-cell malignancy that originates from B cells latently infected with Kaposi’s sarcoma-associated herpesvirus (KSHV, also known as human herpesvirus-8, HHV8). Our previous data indicated that several exogenous ceramide and dh-ceramide species, such as C18-Cer and dhC16-Cer, also displayed effective anti-cancer activities for KSHV+ PEL in vitro and in vivo. However, the underlying mechanisms for exogenous ceramide “killing” PEL cells still require further investigation, which will be helpful to better understand PEL pathogenesis and identify more potential therapeutic targets. In the current study, we used Illumina microarray to determine the altered gene profile in KSHV+ PEL cell-line, BCBL-1 exposure to dhC16-Cer.

2017-06-10 | GSE90038 | 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

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

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

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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