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Transcriptional profiling of HEPG2 cells after treatment with TRIB1-inducing compounds

ABSTRACT: Treatment of HEPG2 cells with TRIB1-inducing compounds and Oncostatin M Transcriptional response of HEPG2 cells was measured after treatment with TRIB1-inducing compound BRD8518 and Oncostatin M, compared to DMSO control treatment at 1, 6 and 24 hours.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57753 | GEO | 2014/12/31

SECONDARY ACCESSION(S): PRJNA248003

REPOSITORIES: GEO

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Homo sapiens

Project description:Transcriptional profiling of HEPG2 cells after treatment with TRIB1-inducing compounds

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Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [array]

Project description:The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBPa, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. Here we provide evidence that Trib1 modulates Hoxa9-associated super-enhancers. ChIP-seq analyses identified increased Histone H3K27Ac signals at the super-enhancers such as Erg, Aff3, Spns2 and Coro2 loci, as well as increased mRNA expression of these genes. The modification of super-enhancer activities is mostly achieved by degradation of C/EBPa by Trib1 and the MEK/ERK pathway only slightly contributes to the activities. Silencing of Erg abrogates the growth advantage acquired by Trib1 overexpression, indicating that Erg is a critical downstream target of the Trib1/Hoxa9 axis. Moreover, treatment of AML cells with the BRD4 inhibitor JQ1 showed growth inhibition in the Trib1/Erg-dependent manner. Upregulation of ERG by TRIB1 was also observed in human AML cell lines, suggesting that Trib1 is a potential target of Hoxa9-associated AML. We used microarrays to detail the global program of gene expression in mouse AML

2020-10-21 | GSE139641 | GEO

Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [ChIP-seq]

Project description:The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBP, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. Here we provide evidence that Trib1 modulates Hoxa9-associated super-enhancers. ChIP-seq analyses identified increased Histone H3K27Ac signals at the super-enhancers such as Erg, Aff3, Spns2 and Coro2 loci, as well as increased mRNA expression of these genes. The modification of super-enhancer activities is mostly achieved by degradation of C/EBP by Trib1 and the MEK/ERK pathway only slightly contributes to the activities. Silencing of Erg abrogates the growth advantage acquired by Trib1 overexpression, indicating that Erg is a critical downstream target of the Trib1/Hoxa9 axis. Moreover, treatment of AML cells with the BRD4 inhibitor JQ1 showed growth inhibition in the Trib1/Erg-dependent manner. Upregulation of ERG by TRIB1 was also observed in human AML cell lines, suggesting that Trib1 is a potential target of Hoxa9-associated AML.

2020-10-21 | GSE140313 | GEO

TRIB1 suppression on human hepatocytes transcriptome

2015-04-13 | GSE61473 | GEO

TRIB1 suppression on human hepatocytes transcriptome

Project description:The TRIB1 locus has been associated with lipid dysfunction. The underlying mechanisms were investigated by examining the transcription landscape in response to TRIB1 suppression in human primary hepatocytes. Primary hepatocytes from 3 distinct donors were exposed for 48 h to an antisense nucleotide targeting TRIB1 or a control nucleotide. The resulting impacts on the transcription profile were assessed using Human Transcriptome 2.0 microarrays (Affymetrix).

2015-04-13 | E-GEOD-61473 | biostudies-arrayexpress

Expression data of GMP and MDP from wild-type and Trib1-/- mice

2013-01-18 | GSE43563 | GEO

Expression data of GMP and MDP from wild-type and Trib1-/- mice

Project description:Trib1 is critical for some myeloid cell differentiation. Therefore we used microarrays to investigate gene expression profiles in wild-type and Trib1-/- progenitor of myeloid cells. Progenitor cells, such as GMP and MDP, obtained from wild-type and Trib1-/- mice were sorted, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2013-01-18 | E-GEOD-43563 | biostudies-arrayexpress

Transcription profiling of mouse Trib1-deficient animals vs controls

Project description:The purpose of this experiment was to compare the gene expression pattern between wild-type and Trib1-deficient macrophages in response to LPS. Experiment Overall Design: Two samples to define LPS-inducible gene and 4 samples (2 for wild-type and the rests for Trib1-deficient mice) for comparison.

2008-11-06 | E-GEOD-8788 | biostudies-arrayexpress

Expression Profiles of HepG2 cells treated with 22 compounds and solvent controls

Project description:The transcriptomics changes induced in the human liver cell line HepG2 by 17 hepatotoxic compounds, 5 non-hepatotoxic compounds and solvent controls after treatment for 24h The study investigated differential gene expression in HepG2 cell line mRNA following 24 hours of exposure to 17 hepatotoxic compounds, 5 non-hepatotoxic compounds and solvent controls. Three biological replicates per compound/solvent. In total 105 arrays .

2014-02-14 | E-GEOD-51952 | biostudies-arrayexpress

Trib1 regulates mouse LDL metabolism through Cebpa-mediated regulation of the LDL receptor in hepatocytes.

Project description:The Tribbles homolog 1 protein (TRIB1), encoded by the gene TRIB1, has been identified by genome-wide association studies (GWAS) as likely to be causal of a remarkable number of cardiometabolic traits, including plasma lipids, hepatic steatosis, adiponectin levels, and coronary artery disease. In its best-known function, Tribbles 1 interacts with the ubiquitin ligate COP1 protein to target the transcription factors CCAAT/enhancer-binding protein alpha and beta (CEBP a/b) for proteasomal degradation. We have previously published that specific Trib1 deletion in mice increased de novo lipogenesis, hepatic steatosis, and plasma triglycerides, attributable at least in part to increased protein levels of hepatic Cebpa. However, the mechanism by which Trib1 regulates plasma lipids and specifically LDL-C metabolism remained unknown. In this experiment our aim was to identify possible molecular interactions by which hepatic Trib1 regulates specifically LDL-C metabolism dependently of Cebpa expression. To do this, we compared total gene expression in livers of wild type mice, Trib1, Cebpa and Trib1;Cebpa hepatic deleted mice. Gene expression data was then used in Ingenuity Pathway analysis to identify upstream transcription factors that might be responsible for the gene expression changes observed.

2023-09-29 | GSE158815 | GEO

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