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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse lymphomagenesis induced by conditional expression of transgenic c-Myc oncogene in six different tumor cell lines

ABSTRACT: Lymphomagenesis was induced by conditional expression of transgenic c-Myc oncogene. Profile of genes expressed in tumor cells was compared with profile of genes in the same cell line treated for 12 hours with doxycycline to abrogate expression of transgenic c-Myc. Six different tumor cell lines were tested.

ORGANISM(S): Mus musculus

SUBMITTER: Dragan Marinkovic

PROVIDER: E-MEXP-169 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identification of novel Myc target genes with a potential role in lymphomagenesis.

Marinkovic Dragan D Marinkovic Tatjana T Kokai Eniko E Barth Thomas T Möller Peter P Wirth Thomas T

Nucleic acids research 20041011 18

The c-Myc transcription factor regulates a wide set of genes involved in processes such as proliferation, differentiation and apoptosis. Therefore, altered expression of Myc leads to deregulation of a large number of target genes and, as a consequence, to tumorigenesis. For understanding Myc-induced transformation, identification of these target genes is essential. In this study, we searched for Myc target genes involved in lymphomagenesis using different mouse T and B cell lymphoma cell lines t ...[more]

PMID: 15477387

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Pcgf6 suppresses Myc-induced lymphomagenesis

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Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [Lymphoma].

Project description:Myc oncoproteins directly regulate transcription by binding to target genes, yet this only explains a fraction of the genes affected by Myc. mRNA turnover is controlled via AU-binding proteins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts. Analyses of precancerous and malignant Myc-expressing B cells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs. Notably, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP, and this circuit is also operational during B lymphopoiesis and IL7 signaling. Importantly, TTP suppression is a hallmark of cancers with MYC involvement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the malignant state. Further, there is a selection for TTP loss in malignancy; thus, TTP functions as a tumor suppressor. Finally, Myc/TTP-directed control of select cancer-associated ARED genes is disabled during lymphomagenesis. Thus, Myc targets AUBPs to regulate ARED genes that control tumorigenesis. Lymphomas collected from EÎ¼-Myc and EÎ¼-Myc;EÂµ-TTP-1 transgenic mice were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430 2.0 Affymetrix arrays.

2012-08-01 | E-GEOD-37790 | biostudies-arrayexpress

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2015-05-19 | E-GEOD-61637 | biostudies-arrayexpress

Regulation of the core pre-mRNA splicing machinery by MYC and PRMT5 is essential to sustain lymphomagenesis [B-cells]

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Regulation of the core pre-mRNA splicing machinery by MYC and PRMT5 is essential to sustain lymphomagenesis [fetal liver]

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Synergy between PI3K Signaling and MYC in Burkitt Lymphomagenesis

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