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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling of HT-29 cells stimulated with pairwise combinations of TNF, EGF, and insulin

ABSTRACT: The objective of this study was to investigate the link between signaling-network activation and transcriptional regulation downstream of tumor necrosis factor (TNF), epidermal growth factor (EGF), and insulin. Microarrays were used to capture the transcriptional responses to TNF, EGF, and insulin at intermediate-to-late times after stimulation. Nine combinations of TNF, EGF, and insulin were evaluated at three time points after stimulation in biological duplicate.

ORGANISM(S): Homo sapiens

SUBMITTER: Kevin Janes

PROVIDER: E-GEOD-69639 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TNF-insulin crosstalk at the transcription factor GATA6 is revealed by a model that links signaling and transcriptomic data tensors.

Chitforoushzadeh Zeinab Z Ye Zi Z Sheng Ziran Z LaRue Silvia S Fry Rebecca C RC Lauffenburger Douglas A DA Janes Kevin A KA

Science signaling 20160607 431

Signal transduction networks coordinate transcriptional programs activated by diverse extracellular stimuli, such as growth factors and cytokines. Cells receive multiple stimuli simultaneously, and mapping how activation of the integrated signaling network affects gene expression is a challenge. We stimulated colon adenocarcinoma cells with various combinations of the cytokine tumor necrosis factor (TNF) and the growth factors insulin and epidermal growth factor (EGF) to investigate signal integ ...[more]

PMID: 27273097

Similar Datasets

Transcriptional profiling of HT-29 cells stimulated with pairwise combinations of TNF, EGF, and insulin

Project description:The objective of this study was to investigate the link between signaling-network activation and transcriptional regulation downstream of tumor necrosis factor (TNF), epidermal growth factor (EGF), and insulin. Microarrays were used to capture the transcriptional responses to TNF, EGF, and insulin at intermediate-to-late times after stimulation.

2016-07-25 | GSE69639 | GEO

Transcriptional profiling of inducible GATA6L-overexpressing HT-29 cells stimulated with TNF

Project description:The objective of this study was to investigate the role of GATA6L with or without TNF stimulation. Microarrays were used to capture the transcriptional response to GATA6L overpexression at intermediate times after TNF stimulation. Cells were induced for GATA6L overexpression and evaluated at two hours after stimulation with saturating TNF in biological triplicate.

2016-07-25 | E-GEOD-72079 | biostudies-arrayexpress

Transcription profiling of human MCF10A mammary gland epithelial cells stimulated with epidermal growth factor vs unstimulated and sampled at multiple time points to investidage the temporal regulation of the cellular EGFR cascade

Project description:MCF10A cells derived from spontaneously immortalized normal human mammary epithelia were subjected to EGF/SERUM stimulation for 0,20,40,60,120,240 and 480 minutes. We used microarrays to understand the temporal regulation of the cellular EGFR cascade. Experiment Overall Design: MCF10A cells were grown in DME:F12 medium supplemented with antibiotics, [10 mg/ml insulin, 0.1 mg/ml cholera toxin, 0.5 mg/ml hydrocortisone, heat-inactivated horse serum (5%); defined as 'serum' in the text] and 10ng/ml EGF. Cells were serum deprived for 24 hours. Following stimulation with EGF/SERUM for 0,20,40,60,120,240 and 480 minutes.

2007-11-01 | E-GEOD-6784 | biostudies-arrayexpress

Homo sapiens

Project description:MCF7 EGF, HRG stimulation

| PRJNA112545 | ENA

Homo sapiens

Project description:H1299 EGF and Iressa stimulation

| PRJNA106031 | ENA

iRhom2 Promotes Lupus Nephritis through ADAM17-Dependent TNF-α and EGFR Signaling

Project description:Lupus nephritis (LN) often results in progressive renal dysfunction. The inactive Rhomboid 2 (iRhom2) is a newly identified key regulator of A disintegrin and metalloprotease 17 (ADAM17), whose substrates, such as TNF-α and heparin-binding EGF (HB-EGF), have been implicated in the pathogenesis of chronic kidney disease. Here we demonstrate that deficiency of iRhom2 protects the lupus-prone Fcgr2b-/- mice from developing severe kidney damage without altering anti-double stranded (ds) DNA Ab production, by simultaneously blocking the HB-EGF/EGFR and the TNF-α signaling in the kidney tissues. Unbiased transcriptome profiling of kidneys and kidney macrophages revealed that TNF-α and HB-EGF/EGFR signaling pathways are highly upregulated in Fcgr2b-/- mice; alterations that were diminished in the absence of iRhom2. Pharmacological blockade of either TNF-α or EGFR signaling protected Fcgr2b-/- mice from severe renal damage. Finally, kidneys from LN patients showed increased iRhom2 and HB-EGF expression, with interstitial HB-EGF expression significantly associated with chronicity indices. Our data suggest that activation of iRhom2/ADAM17-dependent TNF-α and EGFR signaling plays a crucial role in mediating irreversible kidney damage in LN, thereby uncovering a novel target for selective and simultaneous dual inhibition of two major pathological pathways in the effector arm of the disease.

2019-01-01 | GSE107705 | GEO

Homo sapiens

Project description:Dynamic response of EGF stimulation in lung cancer cells [EGF]

| PRJNA328017 | ENA

HiSeeker: Detecting High-Order SNP Interactions Based on Pairwise SNP Combinations.

Project description: Not available

| S-EPMC5485517 | biostudies-literature

Prediction of ultra-high-order antibiotic combinations based on pairwise interactions.

Project description: Not available

| S-EPMC6370231 | biostudies-literature

Free fatty acids and TNF-alpha in HepG2 cell culture

Project description:The regulation of complex cellular activities in palmitate treated HepG2 cells, and the ensuing cytotoxic phenotype, involves cooperative interactions between genes. While previous approaches have largely focused on identifying individual target genes, elucidating interacting genes has thus far remained elusive. We applied the concept of information synergy to reconstruct a ?gene-cooperativity? network for palmititate-induced cytotoxicity in liver cells. Our approach integrated gene expression data with metabolic profiles to select a subset of genes for network reconstruction. Subsequent analysis of the network revealed insulin signaling as the most significantly enriched pathway, and desmoplakin (DSP) as its top neighbor. We determined that palmitate significantly reduces DSP expression, and treatment with insulin restores the lost expression of DSP. Insulin resistance is a common pathological feature of fatty liver and related ailments, whereas loss of DSP has been noted in liver carcinoma. Reduced DSP expression can lead to loss of cell-cell adhesion via desmosomes, and disrupt the keratin intermediate filament network. Our findings suggest that DSP expression may be perturbed by palmitate and, along with insulin resistance, may play a role in palmitate induced cytotoxicity, and serve as potential targets for further studies on non-alcoholic fatty liver disease (NAFLD). free fatty acids(palmitate, oleate, linoleate) 0.7mM and tnf-alpha (0 20,100 ng/ml) were subjected to HepG2 cell line to study the cytotoxicity induced by these two factors. control(Hepg2 medium and BSA medium) treatment(combinations of TNFa+FFAs) two biological replicates for each condition, color swap for each sample

2012-05-01 | E-GEOD-26885 | biostudies-arrayexpress

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