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Identification of Myc-regulated microRNAs in mouse B cell lymphomas

ABSTRACT: We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. miRNA expression was assayed in a murine model of Myc-induced B cell lymphoma. In this system, bone marrow from p53-/- mice is infected with a retrovirus that produces a Myc-estrogen receptor fusion protein (MycER). Infected cells form polyclonal B cell lymphomas in the presence of 4-hydroxytamoxifen (4-OHT), which activates the MycER fusion protein. RNA from subcutaneous tumors with high Myc activity (animals treated continuously with 4-OHT) and low Myc activity (animals in which 4-OHT was withdrawn after tumor formation) was analyzed. Keywords: Dose Response

ORGANISM(S): Human gammaherpesvirus 8 Mus musculus human gammaherpesvirus 4 Murid gammaherpesvirus 4 Human betaherpesvirus 5 Caenorhabditis elegans

PROVIDER: GSE9104 | GEO | 2007/12/05

SECONDARY ACCESSION(S): PRJNA105223

REPOSITORIES: GEO

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Identification of Myc-regulated microRNAs in mouse B cell lymphomas

Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. miRNA expression was assayed in a murine model of Myc-induced B cell lymphoma. In this system, bone marrow from p53-/- mice is infected with a retrovirus that produces a Myc-estrogen receptor fusion protein (MycER). Infected cells form polyclonal B cell lymphomas in the presence of 4-hydroxytamoxifen (4-OHT), which activates the MycER fusion protein. RNA from subcutaneous tumors with high Myc activity (animals treated continuously with 4-OHT) and low Myc activity (animals in which 4-OHT was withdrawn after tumor formation) was analyzed. Keywords: Dose Response RNA from 2 subcutaneous MycER tumors with high Myc activity (animals treated continuously with 4-OHT) and 2 tumors with low Myc activity (animals in which 4-OHT was withdrawn after tumor formation) was analyzed.

2010-05-22 | E-GEOD-9104 | biostudies-arrayexpress

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A high resolution analyis of c-Myc-regulated gene expression dynamics.

Project description:We profiled the transcriptome of HOMycER12 rat fibroblasts whose c-Myc activity was induced to supra-physiological levels with 4-hydroxytamoxifen (OHT). In this dataset, we included the expression data hourly for the first 6 h, then every 2 or 4 hours over a total of 24 h for 4-hydoxytamoxifen activated cells, and expression data from control samples (no 4-hydroxytamoxifen activation) at 8, 16 and 24 h.

2011-11-21 | GSE20550 | GEO

RNA-seq analysis of MCF-10A human mammary epithelial cells following MYC activation

Project description:We profiled gene expression and splicing changes in MCF-10A human mammary epithelial cells expressing MYC fused to a portion of estrogen receptor (MYC-ER) (Eilers et al., 1989; Littlewood et al., 1995). We performed RNA-seq, in triplicate, on 3D-grown MCF-10A MYC-ER cells at 0, 8, and 24 hours (h) after 4-OHT-induced MYC activation. As a control for 4-OHT-induced effects, 3D-grown parental MCF-10A cells lacking the MYC-ER fusion protein were treated with 4-OHT at the same timepoints.

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RNAseq analysis of Human endothelial TeloHAEC in response to Estradiol, 4-hydroxytamoxifen and the cotreatment

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RNAseq of cell line from pancreas from KRasG12D/RosaMycER mouse treated with Tamoxifen

Project description:Experiment designed to study the effect of deregulated myc on pancreatic cancer progression and regression. In the KRasG12D/RosaMycER mouse model KRas and MycER are expressed exclusively in the pancreas, but MycER activity depends on Tamoxifen presence. For this experiment a mouse was treated with Tamoxifen during 3 weeks, the pancreas was collected and the epithelial cells were grown in vitro in the presence of 4-OHT (4-Hydroxytamoxifen, active form of Tamoxifen). RNAseq were preformed on the cell line treated as follows: 1- 4-OHT all the time. 2- EtOH 6h. 3- EtOH 12h. 4- EtOH 18h.

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Transcription profiling by array of mouse promyelocyte granulocytes with activated MYC-ER protein

Project description:The mouse promyelocyte (MPRO) granulocyte cell model expressing the MYC-ER fusion protein encoding transgene was used as a system to perform gene expression profiling in a granulocytic cell setting of low endogenous MYC expression (differentiated MYC-ER MPROs, D4) where we then activated the MYC-ER protein for 24 h with 4-OHT (D5T) as compared to a EtOH vehicle treated control (D5E).

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Transcription profiling of human cells expressing FoxM1-ER fusion protein

Project description:Experiment description To identify FoxM1-regulated genes, we carried out gene expression profile analysis after inducible activation of a FoxM1-ER fusion protein using high-density human cDNA microarrays. We constructed a stable line of U2OS cells expressing full-length HA-FoxM1 fused at its C-terminus to the ligand-binding domain of the estrogen receptor (ER), mutated such that it specifically responds to 4-hydroxytamoxifen (4-OHT) but not to estrogen. In the absence of 4-OHT the activity of the ER fusion protein is turned off, but can be rapidly induced when cells are exposed to 4-OHT. We isolated total RNA from untreated cultures and cultures treated with 4-OHT for 6 or 16 hr. As activation of FoxM1 results in accumulation of cells in G2/M, we additionally analyzed the induction of gene expression by FoxM1 in G1/S-synchronized cells by a thymidine block. Total RNA derived from untreated or stimulated FoxM1-ER cells was amplified, reverse transcribed, labeled and hybridized to cDNA microarrays containing 18,000 cDNAs and expressed sequence tags (ESTs). Bound cDNA was detected using Cy3 or Cy5 dyes. In each independent experiment we included reverted color controls (Cy3 (4-OHT treated); Cy5 (untreated) or Cy3 (untreated); Cy5 (treated)) and the expression profile was expressed as a Cy5:Cy3 ratio.

2005-01-01 | E-MEXP-230 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

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