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Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA or MYB shRNA lentivirus-mediated transduction

ABSTRACT: Human Burkitt's lymphoma ST486 cells were transduced with non-target control shRNA lentiviral vectors, FOXM1 shRNA, and MYB shRNA lentiviral vectors. Total RNA was isolated 24h later. cRNA was produced with the standard one-step IVT protocol (Affymetix) and hybridized in U95Av2 gene chips (Affymetrix).

ORGANISM(S): Homo sapiens

PROVIDER: GSE17172 | GEO | 2009/07/27

SECONDARY ACCESSION(S): PRJNA119665

REPOSITORIES: GEO

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Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA or MYB shRNA lentivirus-mediated transduction

Project description:Human Burkitt's lymphoma ST486 cells were transduced with non-target control shRNA lentiviral vectors, FOXM1 shRNA, and MYB shRNA lentiviral vectors. Total RNA was isolated 24h later. cRNA was produced with the standard one-step IVT protocol (Affymetix) and hybridized in U95Av2 gene chips (Affymetrix). Experiment consists in 3 independent samples: Expression profiling of Burkitt's lymphoma cells 24h after non-target control shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after MYB shRNA lentiviral mediated transduction. Data processing performed using MAS5 or GCRMA.

2009-07-27 | E-GEOD-17172 | biostudies-arrayexpress

Gene expression data following Cyclin T2 and Cyclin T1 depletion by shRNA in HeLa cells

Project description:We have characterized gene expression changes in HeLa cells following long term depletion of Cyclin T2 or Cyclin T1 using shRNA HeLa cells were transduced with VSV-G pseudotyped lentiviral vectors expressing shRNA against either Cyclin T2 or Cyclin T1. As a control, cells were transduced with shRNA vector with four nucleotides mismatch in the Cyclin T1 mRNA that has been previously shown to have minimal effects on mRNA expression levels. The vectors have a GFP reporter that can be used to estimate transduction efficiency. Five days post-transduction, cells were harvested and total RNA extracted. Transcriptional profiling was carried out on these RNA samples. Two independent biological replicate experiments were carried out in this analysis and the xpression values normalized by GC-RMA and averaged. The following comparisons were made: MM to Cyclin T2 and MM to Cyclin T1.

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Project description:We found that FOXO1 knock-down inhibits cell cycle progression in Burkitt's lymphoma (BL) cell lines BL41 and Namalwa.

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Expression profiling of WM9 and 1205Lu with shILEI.

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RNAseq analysis of USP7 knockdown in MM16 and MM27 metastatic melanoma PDX cells

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HCT116 cells N-BLR shRNA vs. empty vector control

Project description:HCT116 cells transfected with lentiviral vectors expressing two different N-BLR shRNAs (clones #3-1 and #4-7) and empty vector control

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circRNA microarray of the Epstein-Barr virus positive Burkitt's lymphoma cell line Akata

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Transcriptomic analysis of TFEB knockdown in LT-HSC.

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Expression data from oral squamous cell carcinoma cell line Cal27 after lentivirus shIL-1beta transfection

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Deep sequencing of MYC DNA-binding sites in Burkitt's lymphoma

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 Burkitt´s lymphoma biology.

2011-11-28 | GSE30726 | GEO

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