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Genome-wide characterization of the transcriptional program of Myc-dependent transformation, expression study

ABSTRACT: We profiled Myc binding in a normal breast cell-line (MCF10A) under basal conditions after ectopic expression of Myc. We showed that ectopic Myc expression increases tumour formation in vivo and in vitro. We then profiled genome-wide Myc binding using Agilent promoter arrays in MCF10A cells expressing wild-type and ectopic Myc. We show that Myc binds to a greater number of spots in wild-type than in Myc cells, but that some targets are unique to each condition. Keywords: genetic-modification and stress-response We compared ectopic Myc to wild-type cells under wild-type and serum-deprived conditions with 4 replicates per condition

ORGANISM(S): Homo sapiens

SUBMITTER: Paul Boutros

PROVIDER: E-GEOD-14263 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide characterization of the transcriptional program of Myc-dependent transformation

Project description:We profiled Myc binding in a normal breast cell-line (MCF10A) under basal conditions after ectopic expression of Myc. We showed that ectopic Myc expression increases tumour formation in vivo and in vitro. We then profiled genome-wide Myc binding using Agilent promoter arrays in MCF10A cells expressing wild-type and ectopic Myc. We show that Myc binds to a greater number of spots in wild-type than in Myc cells, but that some targets are unique to each condition. This SuperSeries is composed of the following subset Series: GSE13749: Genome-wide characterization of the transcriptional program of Myc-dependent transformation, ChIP-chip GSE14263: Genome-wide characterization of the transcriptional program of Myc-dependent transformation, expression study Refer to individual Series

2009-11-24 | E-GEOD-14264 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms (BeadChip)

Project description:Global miRNA expression profiling of human malignancies is gaining popularity in both basic and clinically driven research. But to date, the majority of such analyses have used microarrays and quantitative real-time PCR. With the introduction of digital count technologies, such as next-generation sequencing (NGS) and the NanoString nCounter System, we have at our disposal, many more options. To make effective use of these different platforms, the strengths and pitfalls of several miRNA profiling technologies were assessed, including a microarray platform, NGS technologies and the NanoString nCounter System. These results were compared to gold-standard quantitative real-time PCR. Comparison of non-small cell lung cancer cell lines grown in vitro (n = 5) and in vivo (n = 5) as xenograft models.

2013-10-22 | E-GEOD-51501 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms (NanoString)

2013-10-22 | E-GEOD-51504 | biostudies-arrayexpress

Comparison of microRNA Profiling Platforms

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-22 | E-GEOD-51508 | biostudies-arrayexpress

Genome-wide characterization of the transcriptional program of Myc-dependent transformation, ChIP-chip

2009-11-24 | GSE13749 | GEO

Genome-wide characterization of the transcriptional program of Myc-dependent transformation, expression study

2009-11-24 | GSE14263 | GEO

Genome-wide characterization of the transcriptional program of Myc-dependent transformation

2009-11-24 | GSE14264 | GEO

CD133- HCC cells infected with miR-130b vs. empty vector control

Project description:To identify candidate downstream mRNA target for hsa-miR-130b miR-130b or empty vector control was overexpressed in PLC8024 CD133- HCC cells using lentivirus

2010-12-10 | E-GEOD-17386 | biostudies-arrayexpress

Expression data comparing LNCaP cells infected with miR-616 vs. empty vector control

Project description:To identify candidate downstream mRNA target(s) for hsa-miR-616 Affymetrix Human Genome U133 Plus GeneChip 2.0 miR-616 or empty vector control was stably overexpressed in LNCaP prostate cells using lentivirus

2011-01-15 | E-GEOD-20543 | biostudies-arrayexpress

Oncogenic Ras inhibits IRF1 to promote viral oncolysis

Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).

2014-11-13 | E-GEOD-49469 | biostudies-arrayexpress

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