Increased RNA Polymerase Activity at CTCF binding sites on the Epstein Barr Virus Genome During Reactivation from Latency
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE188584 | GEO | 2023/01/06
REPOSITORIES: GEO
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Project description:Epstein-Barr virus positive Burkitt's lymphoma cell line Akata (+) and it's EBV-depleted subclone Akata (-) were analyzed for human circRNA expression.
2022-12-19 | GSE206824 | GEO
Project description:Epstein-Barr virus (EBV) reactivation in latently infected B cells is essential for persistent infection and B cell receptor (BCR) activation is a physiologically relevant stimulus for EBV reactivation. Post-translational modifications, such as phosphorylation and ubiquitination, are known to be regulated by antigen binding to BCR within minutes. However, a detailed understanding of the signaling alterations at later time when EBV is being actively replicated remains elusive. To gain insights into BCR activation-mediated reprogramming of the cellular environment in both Akata-BX1 (EBV+) and Akata-4E3 (EBV-) B cells, we utilized a 3-plex stable isotope labeling by amino acid in cell culture (SILAC)-based quantitative proteomic approach to monitor the dynamic changes of protein ubiquitination during the course of immunoglobulin G (IgG) cross-linking of BCRs. We observed temporal alterations in the level of ubiquitination on approximately 150 sites in both Akata-BX1 (EBV+) and Akata-4E3 (EBV-) B cells post-IgG cross-linking compared with no cross-linking controls, with the majority of protein ubiquitination down-regulated. Our analysis revealed that IgG cross-linking plays a major role in the regulation of protein ubiquitination in both EBV+ and EBV- B cells. Bioinformatic analyses of up-regulated ubiquitination events revealed significant enrichment of proteins involved in RNA processing. Among the down-regulated ubiquitination events are proteins enriched in apoptosis and the ubiquitin-proteasome pathway. The comparative and quantitative studies provide a foundation for further understanding how BCR activation regulates cellular protein ubiquitination and how EBV utilizes or subverts BCR engagement-mediated changes to facilitate viral replication.
2017-02-02 | PXD004562 | Pride
Project description:Using strand specific RNA-seq to assess the EBV transcriptome during reactivation of Akata cells, we found extensive bidirectional transcription extending across nearly the entire genome. Illumina strand-specific RNA-seq of BCR-activated Akata cells at 9 time points
2013-12-24 | E-GEOD-52490 | biostudies-arrayexpress
Project description:Transition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV. Keywords: Disease state analysis We used Affymetrix microarrays to examine variations in global gene expression between the paired EBV-positive (1B6) and EBV-negative (2A8) Akata Burkitt's lymphoma clones. EBV-negative Akata clones were generated by treatment with hydroxyurea, an inhibitor of ribonucleotide reductase that forced rapid loss of EBV episomes and compared to their EBV-positive counterparts. Logarithmically growing EBV-negative and positive Akata EBV clones were seeded at 2.5x10^5 cells/ml in RPMI1640 supplemented with 10% fetal bovine serum, 2mM glutamine, and 100units/ml penicillin/streptomycin. The next day, the cells were incubated for 4 hours in media containing 1% fetal bovine serum (low serum), 2mM glutatmine and 100units/ml penicillin/streptomycin to begin selection of the Akata tumor phenotype. The short incubation time was intended to minimize cell death and other potential downstream effects of low serum treatment, while at the same time initiating expression changes contributing to the tumorigenic phenotype.
2010-01-19 | E-GEOD-19761 | biostudies-arrayexpress
Project description:The Epstein-Barr virus (EBV) is associated with lymphoid and epithelial cancers. Initial EBV infection alters lymphocyte gene expression, inducing cellular proliferation and differentiation as the virus transitions through consecutive latency transcription programs. Cellular microRNAs (miRNAs) are important regulators of signaling pathways and are implicated in carcinogenesis. The extent to which EBV exploits cellular miRNAs is unknown. Using micro-array analysis and quantitative PCR, we demonstrate differential expression of cellular miRNAs in type III versus type I EBV latency including elevated expression of miR-21, miR-23a, miR-24, miR-27a, miR-34a, miR-146a and b, and miR-155. In contrast, miR-28 expression was found to be lower in type III latency. The EBV-mediated regulation of cellular miRNAs may contribute to EBV signaling and associated cancers. There were two major objectives for this study. The first objective was to determine whether EBV infected cells exhibiting type I latency influence cellular microRNA expression. For this study, four EBV negative derivatives of the type I latency cell line, Mutu I, were derived by retroviral infection with a dominant negative from of the EBV episomal replication factor, EBNA1. RNA from these four clones were compared to parental EBV positive Mutu I cells. Four dual labeling experiments were carried out for this comparison with dye reversal for every second pair of RNAs. The second objective was to determine whether EBV type III latency cells exhibit altered cellular microRNA gene expression compared to type I latency cells or EBV negative B cells. Four dual labeling experiments were carried out for this analysis with dye reversal for every second pair of RNAs.
2010-05-19 | E-GEOD-13056 | biostudies-arrayexpress
Project description:Using strand specific RNA-seq to assess the EBV transcriptome during reactivation of Akata cells, we found extensive bidirectional transcription extending across nearly the entire genome.
2013-12-24 | GSE52490 | GEO
Project description:Seroepidemiological studies imply a correlation between Epstein-Barr virus (EBV) reactivation and the development of nasopharyngeal carcinoma (NPC). Phorbol esters, butyrates and N-nitroso compounds are known chemical carcinogens in foodstuffs and cigarettes that have been implicated as risk factors contributing to the development of NPC. We have demonstrated previously that low dose N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, 0.1 microg/ml) had a synergistic effect with 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate (SB) in enhancing EBV reactivation (Chem Biol Interact 188: 623-634). Since residents of areas with a high risk of NPC are reported to contact with these carcinogens (TPA, SB or nitrosamines) frequently, we sought to determine the consequence of repeated exposure of EBV-harboring nasopharyngeal cells to these carcinogens in a long-term, low dose, repeated manner. An NPC cell line latently infected with EBV, NA, was periodically treated with TPA/SB combined with MNNG for recurrent EBV reactivation. After 10 times of chemically-induced recurrent reactivation of EBV, the expression profile analysis indicates that many carcinogenesis-related genes were altered in recurrent reactivated NA cells when compared to the parental NA cells. The expression profile was analyzed in the recurrent EBV reactivated NA cells and the parental NA cells.
2012-08-15 | GSE38453 | GEO
Project description:Seroepidemiological studies imply a correlation between Epstein-Barr virus (EBV) reactivation and the development of nasopharyngeal carcinoma (NPC). Phorbol esters, butyrates and N-nitroso compounds are known chemical carcinogens in foodstuffs and cigarettes that have been implicated as risk factors contributing to the development of NPC. We have demonstrated previously that low dose N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, 0.1 microg/ml) had a synergistic effect with 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate (SB) in enhancing EBV reactivation (Chem Biol Interact 188: 623-634). Since residents of areas with a high risk of NPC are reported to contact with these carcinogens (TPA, SB or nitrosamines) frequently, we sought to determine the consequence of repeated exposure of EBV-harboring nasopharyngeal cells to these carcinogens in a long-term, low dose, repeated manner. An NPC cell line latently infected with EBV, NA, was periodically treated with TPA/SB combined with MNNG for recurrent EBV reactivation. After 10 times of chemically-induced recurrent reactivation of EBV, the expression profile analysis indicates that many carcinogenesis-related genes were altered in recurrent reactivated NA cells when compared to the parental NA cells. The expression profile was analyzed in the recurrent EBV reactivated NA cells and the parental NA cells. The expression profile of two NA cells, NA-P10/TS-MG and NA-P1/mock, were analyzed in this study. NA-P10/TS-MG cells were subject to 10 times of repeated chemical exposure by incubating these cells periodically with TPA/SB (10 ng/ml and 1.0 mM) in combination with MNNG (0.1 microg/ml). The NA cells at the beginning of this experiment were defined as passage 0 (P0) cells. 24 h after seeding, the cells were subjected to a 24 h period of mock or chemical treatment. After this 24 hr treatment, the cells were recovered by replacing the medium with fresh (treatment-free) medium and incubation for a further 48 h. The resulting cells were defined as passage 1 (P1) cells. Cells from P1 were trypsinized and transferred and the process repeated again to obtain the P2 cells. A total of ten treatments were applied to the cells in this study. M-bM-^@M-^\NA-P10/TS-MGM-bM-^@M-^] refers to NA cells with 10 times of combined TPA/SB and MNNG (TS-MG) treatments. NA-P1/mock is mock-treated NA cells with one time of passage that was used as reference in this study. Replicates were included for each samples.
2012-08-14 | E-GEOD-38453 | biostudies-arrayexpress
Project description:We examined the viral epitranscriptome in EBV transformed lymphoblastoid cell lines (LcLs) and EBV-positive Burkitt's lymphoma, Akata cells, using methylated RNA immunoprecipitation followed by sequencing (MeRIP-seq). Biological replicates of ribo-RNA deleted mRNA of each cell type were prepared for MeRIP-seq followed by peak calling using the exome Peak package with settings for stringent peak calling on both strands of the genome.
2023-08-12 | GSE129217 | GEO
Project description:Transition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV. Keywords: Disease state analysis
2010-01-20 | GSE19761 | GEO