Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global proteomic profiles of human lymphoma cells in vitro under Epstein Barr

ABSTRACT: The Epstein-Barr Virus (EBV) encodes viral microRNAs (miRs) that contribute to the pathogenesis of nasopharyngeal and gastric carcinomas, but their potential roles in lymphomas are still to be elucidated. This study sought to assess the impact of knocking down EBV miRs BART 7 and BART9 in EBV-positive Akata cell lines using CRISPR/Cas9 technology and proteomic strategy.

INSTRUMENT(S): Q-Exactive (Thermo Fisher)

ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Epstein-barr

SUBMITTER: Viviana Loureiro Rocha Deilson Elgui de Oliveira Brunno Felipe Ramos Caetano Bruno Cesar Rossini Lucilene Delazari dos Santos

PROVIDER: MSV000090486 | MassIVE | Fri Oct 07 04:08:00 BST 2022

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Differences in gastric carcinoma microenvironment stratify according to EBV infection intensity; implications for possible immune adjuvant therapy

Project description:Our goal of this study was to perform quantitative and global assessment of EBV gene expression in gastric carcinomas and assess EBV associated cellular pathway alterations.

2013-06-23 | GSE45453 | GEO

Differences in gastric carcinoma microenvironment stratify according to EBV infection intensity; implications for possible immune adjuvant therapy

Project description:Our goal of this study was to perform quantitative and global assessment of EBV gene expression in gastric carcinomas and assess EBV associated cellular pathway alterations. Examination of a gastric carcinoma cell line naturally infected with EBV, SNU-719 using poly-A and ribodepletion RNA-seq data sets

2013-06-23 | E-GEOD-45453 | biostudies-arrayexpress

The Histone Demethylase LSD1/ZNF217/CoREST Complex is a Major Restriction Factor of Epstein-Barr Virus Lytic Reactivation

Project description:Epstein-Barr virus (EBV) contributes to ~1.5% of human cancers, including lymphomas, gastric and nasopharyngeal carcinomas. In most of these, nearly 80 viral lytic genes are silenced by incompletely understood epigenetic mechanisms, precluding use of antiviral agents such as ganciclovir to treat the 200,000 EBV-associated cancers/year. To identify host factors critical for EBV latency, we performed a human genome-wide CRISPR-Cas9 screen in Burkitt B-cells. Top hits included the lysine-specific histone demethylase LSD1 and its co-repressors ZNF217 and CoREST. LSD1 removes histone 3 lysine 4 (H3K4) and histone 3 lysine 9 (H3K9) methylation marks to downmodulate chromatin activation. LSD1, ZNF217 or CoREST knockout triggered EBV reactivation, as did a LSD1 small molecule antagonist, whose effects were additive with histone deacetylase inhibition. LSD1 blockade reactivated EBV in Burkitt lymphoma, gastric carcinoma and nasopharyngeal carcinoma models, sensitized cells to ganciclovir cytotoxicity and induced EBV reactivation in murine xenografts. ZNF217 and LSD1 co-occupied the EBV immediate early gene BZLF1 promoter, which drives B-cell lytic cycle, as well as to the oriLyt enhancer regions recently implicated in EBV reactivation. LSD1 depletion increased levels of activating histone 3 lysine 4 (H3K4) methylation but not repressive histone lysine 9 methylation marks at BZLF1 and oriLyt and induced their interaction by long-range DNA looping. An orthogonal CRISPR screen highlighted a key H3K4 methyltransferase KMT2D role in driving EBV reactivation. Our results highlight H3K4 methylation as a major EBV lytic switch regulator and suggest novel therapeutic approaches.

2025-02-19 | GSE284859 | GEO

Effect of GPX4 knockdown on gene expression profile of EBV positive gastric cancer cell line AGS-EBV.

Project description:Reactive oxygen species (ROS) mediated oxidative stress plays an increasingly extensive role in tumorigenesis. Oxidative stress is also an important mechanism for host cells to resist infection by pathogenic microorganisms. Viruses have a similar defense mechanism. Studies have shown that ROS levels are elevated during in vitro and in vivo EBV infection. In nasopharyngeal carcinoma, EBV latent membrane protein LMP1 "REDOX" nasopharyngeal carcinoma cells by up-regulating NRF2 and NOX2, acquiring new REDOX homeostasis to tolerate higher levels of ROS. In gastric cancer, EBV upregulates NOX2 by down-regulating miR34a via EBNA1, thereby enhancing the antioxidant capacity of host cells. In addition, oxidative stress is involved in the lytic reactivation of EBV, but the specific mechanism is not clear. GPX4 is an important ROS scavenger that plays a role in maintaining cellular REDOX homeostasis. Our study showed that GPX4 is relatively highly expressed in EBV-positive gastric cancer cell lines, which can promote tumor proliferation and migration, and we found that GPX4 helps maintain latent infection of EBV in gastric cancer. In order to further explore the specific mechanism, we performed transcriptome sequencing analysis after knocking down GPX4 expression in AGS-EBV cells.

2025-01-16 | GSE286972 | GEO

USP7 inhibitors disrupt EBNA1 interactome and EBV tumorigenesis

Project description:Epstein-Barr virus (EBV) is a ubiquitous human ɣ-herpesvirus implicated in various malignancies, including Burkitt’s lymphoma and gastric carcinomas. In most EBV-associated cancers, the viral genome is maintained as an extrachromosomal episome by the EBV nuclear antigen-1 (EBNA1). EBNA1 is considered to be a highly stable protein that interacts with the ubiquitin-specific protease 7 (USP7), but the precise role of USP7 in controlling EBNA1 stability and function is not fully understood. Here, we show that pharmacological inhibitors and small interfering RNA (siRNA) targeting USP7 reduce EBNA1 protein levels. The USP7 inhibitor GNE6776 altered EBNA1 protein interactions, including disrupting its ability to bind to USP7. GNE6776 also inhibited EBNA1 binding to EBV oriP DNA and reduced viral episome copy number. GNE6776 selectively inhibited EBV+ gastric and lymphoid cell proliferation in cell culture and slowed EBV+ tumor growth in mouse xenograft models. Transcriptomic studies revealed that USP7 inhibition differentially affected EBV+ cancer cells compared to EBV- cells with a significant effect on chromosome segregation and mitotic cell division pathways. Our findings indicate that USP7 inhibition perturbs EBNA1 stability and function and can be exploited to target EBV+ cancer cells selectively.

2025-01-31 | GSE284839 | GEO

Expression data of EBV-positive and EBV-negative subclones of gastric adenocarcinoma cell line AGS

Project description:Gastric cancer is one of the most common cancers worldwide. Epstein-Barr virus-associated gastric cancer accounts for approximately 10% of all gastric cancers. EBV expresses its own proteins and miRNAs (BART miRNAs) and regulates host gene expression. In this study, we examined the effect of EBV infection on host mRNA expression. Differential gene expression was analyzed between EBV-negative human gastric cancer cell line AGS and EBV-positive human gastric cancer cell line AGS-EBV.

2019-10-14 | GSE135644 | GEO

Post-infectious time-series DNA methylation analysis in gastric epithelial cells

Project description:Time-series comprehensive DNA methylation analysis after EBV infection in the immortalised normal gastric epithelial cell line, GES1, and low methylation gastric cancer cell line, MKN7. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 9 GES1 with and without EBV infection, 5 MKN7 with and without EBV infection, EBV+ gastric cancer cell and xenograft, SNU719 and KT, 2 normal gastric mucosae, 2 low-methylation gastric cancer cases, and 2 high-methylation gastric cancer cases.

2017-04-28 | GSE89269 | GEO

Expression data from control and GAPLINC knock down human gastric cancer cell lines

Project description:Transcriptional profiling of comparing control and GAPLINC stable knocking-down human gastric cancer cell lines. Goal was to determine the different gene expression between control and GAPLINC stable knocking-down human gastric cancer cell lines. Control and GAPLINC stable knocking-down human gastric cancer cell lines were prepared for RNA extraction and hybridization on Affymetrix microarrays.

2014-08-19 | E-GEOD-51651 | biostudies-arrayexpress

Aberrant DNA methylation epigenotype expanding to non-polycomb target genes, induced by Epstein-Barr virus infection in human gastric cancer [Illumina Methylation]

Project description:Aberrant promoter methylation is known to be deeply involved in human gastric carcinogenesis, while association of Epstein-Barr virus (EBV) to the aberrant methylation has not been fully clarified. We analyzed promoter methylation in clinical gastric cancer cases using illumina's Infinium beadarray, and hierarchical clustering analysis classified gastric cancer into three subgroups: low and high methylation epigenotypes in EBV-negative cases, and markedly higher methylation epigenotype that was completely matched to EBV-positive cases. Three epigenotypes were characterized by three groups of genes: genes methylated specifically in the EBV-positive epigenotype (EBV(+)-markers, e.g. CXXC4, TIMP2, PLXND1), genes methylated both in EBV-positive and high epigenotypes (High-markers, e.g. COL9A2, EYA1, ZNF365), and genes methylated all in EBV-positive, high and low epigenotypes of gastric cancer (Common-markers, e.g. AMPH, SORCS3, AJAP1). Polycomb repressive complex (PRC)-target genes in ES cells were significantly enriched in High- and Common-markers (P=2x10-15 and 2x10-34, respectively), but not in EBV(+)-markers (P=0.2), suggesting a different cause for EBV(+)-marker methylation. Recombinant EBV was infected to low epigenotype gastric cancer cell, MKN7. In all the three independently established clones, DNA methylation was induced in High- and EBV(+)-markers after 18 weeks, demonstrating that EBV-positive epigenotype should involve methylation of Common-, High-, and EBV(+)-markers simultaneously. The de novo methylated genes were overlapped well among the three clones, and the methylation caused gene repression. In summary, gastric cancer was classified into three DNA methylation epigenotypes, EBV-positive gastric cancer showed markedly high methylation epigenotype expanding to non-PRC target genes, and EBV infection per se could induce the EBV-positive epigenotype.

2012-01-04 | GSE31788 | GEO

Aberrant DNA methylation epigenotype expanding to non-polycomb target genes, induced by Epstein-Barr virus infection in human gastric cancer [Affymetrix Expression]

2012-01-04 | GSE31787 | GEO