The EBV microRNA targetome
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE147228 | GEO | 2020/08/01
REPOSITORIES: GEO
Similar Datasets
Project description:Refractory Cancer (RC) Burkitt’s Lymphoma (BL)
| PRJNA818765 | ENA
Project description:RNAseq was used to identify host and EBV viral transcriptome changes in CHAF1B knock-out Akata EBV+ cells. CHAF1B KO Akata EBV+ cells were subjected to RNAseq analysis. The Akata EBV+ cells expressing control sgRNA was used as the control.
2020-10-15 | GSE148910 | 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
Project description:EBV-positive cell lines were assayed for expression of EBV miRNAs. The names of the miRNAs are from miRBase from Fall 2007. Microarray probes are tandem complements of the mature miRNA sequence. We assayed Burkitt's lymphoma (BL), Nasopharyngeal carcinoma, post-transplant lymphoproliferative disease (PTLD), primary effusion lymphoma, and lymphoblastoid cell lines. We also assayed primary B cells that were infected with the B95-8 strain of EBV, which was found to express EBV miRNAs as early as 20 hours post infection. We have found PTLD and BLs from HIV-positive donors both express EBV miRNAs. These types of cell lines have not previously been found to express viral miRNAs. We have found that cells that support type I and type II latency express only the BART miRNAs, whereas cells that support type III latency express BART and BHRF1 miRNAs. Furthermore, BL cell lines that spontaneously lose EBV express levels of the viral miRNAs that are at least 5-fold lower than cell lines that do not lose EBV. In total, 48 samples have been assayed and included in this study. EBV-negative control samples are not included in this data set, but raw and processed data may be requested from the contributors. These EBV-negative cell lines include the Burkitt's lymphoma cell lines, BJAB and Akata-negative, the gastric carcinoma cell line, AGS, and uninfected primary B cells. Of the 48 samples, we have assayed 22 different EBV-positive cell lines and 4 different time points after infection of primary B cells with EBV. Replicates of the majority of cell lines is included in this data set. Replicates are from independent RNA isolations that were then hybridized to individual microarrays.
2008-11-30 | E-GEOD-12014 | biostudies-arrayexpress
Project description:Burkitt lymphoma (BL) is a highly aggressive B cell non-Hodgkin lymphoma (B-NHL), which originates from germinal center (GC) B cells and harbors translocations deregulating the MYC oncogene. A comparative analysis of microRNAs (miRNAs) expressed in normal and malignant GC B cells identified miR-28 as significantly down-regulated in BL, as well as in other GC-derived B-NHL. We show that re-expression of miR-28 impairs cell growth and clonogenic properties of BL cells by modulating several targets including MAD2L1, a component of the spindle checkpoint whose down-regulation is essential in mediating miR-28-induced growth-arrest, and BAG1, an activator of the ERK pathway.
2014-06-01 | GSE56268 | GEO
Project description:To identify genes mediating tumor transformation we compared the transcriptome of five Burkitt lymphoma (BL) cell lines (tumor cells) with that of a pool of three lymphoblastoid B-cell lines (LCL; immortal, but not tumor cells). Each BL cell line was considered as a biological replicate. BL cell lines: DG-75, Ramos, BL2, Mutu-I and Akata. LCL cell lines: X50-7, IB4 and Dana.
2015-09-30 | GSE41865 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNAs involved in the posttranscriptional regulation of gene expression. Deregulated miRNA levels have been reported in Burkitt lymphoma (BL) compared to normal B cells and a number of miRNA target genes have been identified in BL cell lines. Here, we determined for the first time the miRNA targetomes of primary BL tumors in comparison with normal B cells. AGO2-RNA immunoprecipitation (AGO2-RIP) in two frozen diagnostic BL tissue samples and three CD19+ B-cell samples isolated from routinely removed tonsils revealed distinct miRNA targetomes of BL and normal B cells. Targets of the miR-17~92 cluster were significantly more frequently AGO2-IP enriched in BL while targets of miR-29 and miR-150 were more frequently AGO2-IP enriched in normal B cells. Furthermore, we showed that miRNA target genes in BL are mainly involved in cell cycle and cell death. Immunohistochemistry on BL tumor samples and tonsil tissues confirmed altered protein levels for two out of six selected miRNA targets, in line with the differential AGO2-IP enrichment between BL and normal B cells. A comparison of AGO2-IP enriched genes in primary BL cases with BL cell lines indicated that approximately half of the miRNA targets may be missed in studies using BL cell lines, while almost 60% of miRNA target genes identified in cell lines were not AGO2-IP enriched in primary BL cases. Our results demonstrate both the necessity and feasibility of studying miRNA-target interactions in primary tumors.
2018-01-19 | GSE107325 | GEO
Project description:We report the identification of potential novel RNA targets for box C/D snoRNAs in human HEK293 cells, using the approaches of UV crosslinking and sequencing of hybrids (CLASH), and formaldehyde crosslinking and sequencing of hybrids (FLASH).
2021-07-21 | GSE114825 | 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 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:We report the identification of potential novel RNA targets for box C/D snoRNAs in budding yeast, using the approach of UV crosslinking and sequencing of hybrids (CLASH).
2018-08-17 | GSE114680 | GEO