Gene expression data in DLEU1 downregulated BL cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Sanghoon Lee
PROVIDER: E-GEOD-65674 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Background: MYC is a transcription factor encoded by the c-MYC gene (thereafter termed MYC). MYC is key transcription factor involved in many central cellular processes including ribosomal biogenesis. MYC is overexpressed in the majority of human tumours including aggressive B-cell lymphoma especially Burkitt's lymphoma. Although Burkitt's lymphoma is a highlight example for MYC overexpression due to a chromosomal translocation, no global analysis of MYC binding sites by chromatin immunoprecipitation (ChIP) followed by global next generation sequencing (ChIP-Seq) has been conducted so far in Burkitt's lymphoma. Methodology/Principal Findings: ChIP-Seq was performed with a MYC-specific antibody giving rise to 7,054 predicted MYC binding sites after bioinformatics analysis of a total of 19 million sequence reads. In line with previous findings, binding sites accumulate in gene sets known to be involved in the ribosomal biogenesis, histone acetyltransferase and methyltransferase complexes and the cell cycle demonstrating a regulatory role of MYC in these processes. Unexpectedly, MYC binding sites also accumulate in genes typically expressed in mature B-cells. To assess the functional consequences of altered MYC binding, the ChIP-Seq data were supplemented with siRNA mediated knock-downs of MYC in BL cell lines followed by gene expression profiling. Interestingly, amongst others, genes involved in B-cell function were up-regulated in response to MYC silencing. Conclusion/Significance: The 7,054 MYC-binding sites identified by our ChIP-Seq approach greatly extend the knowledge regarding MYC binding in Burkitt's lymphoma and sheds further light on the enormous complexity of the MYC regulatory network. Especially our observation that (i) many B-cell relevant genes are targeted by MYC and (ii) that MYC down-regulation leads to an up-regulation of B-cell genes highlights an interesting aspect of BurkittM-BM-4s lymphoma biology. [ChIP-Seq] Analysis of MYC DNA binding sites by ChiP-Seq in 5 BurkittM-BM-4s lymphoma cell lines (Raji, Ramos, Blue1, BL41, CA46) [mRNA expression profiling] siRNA-mediated knock-down of MYC was done employing the BL cell lines Raji, BL41 and Blue1 in order to detect MYC-driven gene expression changes. For this purpose, the cells were Amaxa-transfected using MYC smart pool siRNA and control siRNA (Thermo Scientific/Dharmacon, Erembodegem, Belgium), respectively.
2011-11-28 | E-GEOD-30726 | biostudies-arrayexpress
Project description:Comparison of gene expression profiling between DLEU1 downregulated Raji BL cell and wild type Raji BL cell
2015-06-04 | GSE65674 | GEO
Project description:Although therapy responsiveness to therapy in Burkitt lymphoma (BL) is high, relapsed disease and and chemoresistance remain a clinical challenge, and complete mechanisms underlying BL chemoresistance and how it can be circumvented is yet to be fully elucidated. In this study we present data showing that chymotrypsin-like serine proteases inhibitor Nα-tosyl-L-phenylalanine chloromethylketone (TPCK) and specific NF-κB inhibitor Bay-11 7082 can induce caspase-independent apoptosis in chemoresistant BL cells. We also demonstrate that both TPCK and Bay-11 7082-treatment leads to decreased NF-κB nuclear activity and that this is associated with sensitization of chemoresistant Burkitt lymphoma cells. Furthermore we investigated global transcriptional changes induced by Bay-11 7082 and TPCK in the DG-75 and Raji cell lines, respectively, by microarray analysis using Illumina BeadChips. TPCK-treatment of Raji and DG-75 cells resulted in 59 and 21 differently expressed genes, respectively, while Bay-11-treated Raji and DG-75 cells displayed 1403 and 8 differently expressed genes, respectively. Gene Ontology (GO) categorization confirmed enrichment of multiple GOs in Bay 11-treated Raji and DG-75 cells. Fifty percent of the 61 categories in Raji cells were categories sorting under Biological Processes and represented mostly increased gene expression. In DG-75 cells Bay-11 7082 induced significant gene ontology enrichment in only two categories, where the increased/decreased ratio was 1:1. Further unsupervised and supervised bioinformatics processing by Ingenuity Pathway Analysis indicated significant networks in response to TPCK and Bay 11 respectively, including association to NF-κB. Bay-11 7082 demonstrated deregulated NF-κB related members of receptor mediated cell death signaling, i.e TRAF2 and TRADD, as well as deregulated members of the NF-κB signaling pathway from the cytoplasmic compartment, i.e RELB, in Raji cells. Comparably NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK demonstrated deregulation of NF-κB target genes CD69 and IL8. These data indicates that NF-kB may play a role in overcoming chemoresistance in BL cells with defective classical apoptosis signaling. NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK
2014-01-19 | E-GEOD-31258 | biostudies-arrayexpress
Project description:Expression of the TM4SF member CD9 on the human Burkitts lymphoma cell line Raji induced increased cell proliferation, motilty and adhesion to fibronectin. CD9 promoted increases in Raji cell proliferation was dependent upon histone deacetyalase (HDAC) activity as treatment with HDAC inhibitors trichostain A or cucurmin attenuated CD9 mediated increases in Raji cell proliferation. Gene expression of Raji cells stably expressing human CD9 via transfection with expression vector PRVCMVCD9 was compared with corresponding Mock transfected cell by microarray analysis using the Affymetrix U133 2.0 platform. Experiment Overall Design: Transfected Raji cells that had been in cultured in RPMI, 10% FBS in the presence of 1mg/ml G418 were harvested during exponential growth and RNA was extracted using TRiReagent according to manufacturer's protocol (Sigma).
2009-10-27 | E-GEOD-13210 | biostudies-arrayexpress
Project description:Gene expression profiling of Peditric Burkitt lymphoma (PBL) patients samples were performed to analyze the comparative genomic signature and to investigate targetable signaling pathways in PBL 11 primary tumor specimens were obtained from Pediatric Burkitt lymphoma (PBS) patients and samples were hybridized to HGU133A2. Genechip (Affymetrix)
2015-06-04 | E-GEOD-64905 | biostudies-arrayexpress
Project description:In this study we analyzed gene expression profiles in a well-characterized BL cell line upon treatment with HDACi combined with chemotherapy. The impact on gene expression regulation was broader when HDACi was combined with chemotherapy, than when either therapy was used alone. As expected, treatment interfered in the regulation of cell cycle progression and enhanced cell death. Noteworthy was the effect on members of p53 signaling pathway. The down regulation of PI3KCA and up regulation of p16 were observed at the gene and protein levels, while the inhibition of Akt phosphorylation and the down regulation of c-Myc were confirmed through the analysis of protein levels. As a complementary approach we investigated if HDACi combined with chemotherapy treatment would enhance mir-101, mir-143 and mir-145 levels in BL cell line. This hypothesis was confirmed and we also observed that levels of mir-101, mir-143 and mir-145 were extremely down regulated in BL patients' samples. In this study we demonstrate mechanisms involved in cell cycle arrest upon cell treatment using a combination of HDACi and chemotherapy. We highlight the fact that effective combinations of HDACis with other cytotoxic drugs could improve BL therapy in the future. DNA microarrays were used to access global gene expression modulation upon treatment of Raji BL cell line with VP-16 or NaB and a combination of NaB and VP-16 for 24 hours. Total RNA was extracted using TrizolM-BM-.. Gene expression of treated cells was compared with controls consisting of untreated cells. Microarray analysis was performed using Agilent Whole Human Genome Microarray 4M-CM-^W44K arrays and labeled using the One Color Quick Amp Labeling Kit (Agilent Technologies). Two biological replicates were included for each experimental condition.
2014-06-20 | E-GEOD-48399 | biostudies-arrayexpress
Project description:(i) RNA transcripts of Raji iBZLF1 cells (https://www.biorxiv.org/content/10.1101/573659v1) were compared between non-induced cells and cells induced with doxycycline (100 ng/ ml) for 6 h. Human (Hg19) as well as viral (EBV, Raji KF717093.1) transcripts were analyzed. Artificial ERCC Spike-ins (Thermo Scientific) were added to selected samples to control for global changes of RNA levels. (ii) For control purposes, the RNA transcripts in Raji cells equipped with a doxycycline-controlled truncated BZLF1 allele lacking its transactivation domain (Raji iBZLF1 AD-truncated) were prior to and after induction for 6 h. (iii) For another control, the RNA transcripts of parental, unmodified Raji cells were analyzed prior to and after doxycycline induction for 6 h. All experiments were performed as triplicates.
2019-01-01 | E-MTAB-7820 | biostudies-arrayexpress
Project description:Identifying PD-1 interacting proteins in Jurkat cells expressing PD-1 after stimulation with Raji cells and the superantigen SEE.
2019-05-06 | PXD010864 | Pride
Project description:Identifying PD-1 interacting proteins in Jurkat cells expressing PD-1 after stimulation with Raji cells and the superantigen SEE.
2019-05-06 | PXD013531 | Pride
Project description:B-cell receptor (BCR) signaling promotes the survival of malignant B cells, such as Burkitt’s lymphoma (BL) and the activated B-cell-like subtype of diffuse large B cell lymphoma (ABC-DLBCL). In contrast to ABC DLBCL, where malignant cells require chronic activation of the BCR for their survival, BL cells are dependent on tonic BCR signaling that is antigen-independent. Elucidation and systematic comparison of tonic and activated BCR signaling led to the identification of novel signaling effectors, among them ACTN4 and ARFGEF2, which were identified as regulators of BL cell survival. As tonic and activated BCR signaling are relevant for important aspects of B cell biology, our study helps in gaining an understanding of BCR-induced processes not only in malignant but potentially also physiological settings.
2016-05-09 | PXD003492 | Pride