Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of two human colon cancer cell lines treated with n-3 PUFA docosahexaenoic acid for 3 different time points

ABSTRACT: Several studies indicate that omega (n)-3 fatty acids may have a potential in the prevention and treatment of cancer. In this study the colon cancer cell lines SW480 and SW620 were treated with the n-3 PUFA DHA (Docosahexaenoic acid) for 3 different time points (12, 24 and 48h). The experiments were performed in three independent replicates (1-3), RNA isolated and used for Affymetrix gene expression analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Caroline Jakobsen

PROVIDER: E-MEXP-1014 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

DHA induces ER stress and growth arrest in human colon cancer cells: associations with cholesterol and calcium homeostasis.

Jakobsen Caroline Hild CH Størvold Gro Leite GL Bremseth Hilde H Follestad Turid T Sand Kristin K Mack Merete M Olsen Karina Standahl KS Lundemo Anne Gøril AG Iversen Jens Gustav JG Krokan Hans Einar HE Schønberg Svanhild Arentz SA

Journal of lipid research 20080619 10

Polyunsaturated fatty acids (PUFAs) are normal constituents of the diet, but have properties different from other fatty acids (e.g., through generation of signaling molecules). N-3 PUFAs reduce cancer cell growth, but no unified mechanism has been identified. We show that docosahexaenoic acid (DHA; 22:6 n-3) causes extensive changes in gene expression patterns at mRNA level in the colon cancer cell line SW620. Early changes include unfolded protein response (UPR) and increased levels of phosphor ...[more]

PMID: 18566476

Similar Datasets

Transcription profiling of human colon cancer cell line SW620 treated with docosahexaenoic acid

Project description:The human colon cancer cell line SW620 was supplemented with DHA (70 µM) or an equal volume of ethanol (control). Total RNA was isolated after 6 h and used for Affymetrix gene expression profiling.

2009-06-01 | E-MEXP-2010 | biostudies-arrayexpress

Transcription profiling of human colon cancer cell line SW620 treated wit tetradecylthioacetic acid (TTA) or control (NaOH).

Project description:Adenocarcinoma cell line SW620 were treated with tetradecylthioacetic acid,TTA, or control (NaOH) for 24 h. degrees RNA isolated, Affymetrix gene expression

2010-08-31 | E-MEXP-2590 | biostudies-arrayexpress

Transcription profiling of human human neuroblastoma SH-SY5Y cells identifies molecular effectors of unconjugated bilirubin

Project description:This SuperSeries is composed of the following subset Series:; GSE16656: Transcriptome analysis identifies molecular effectors of unconjugated bilirubin in human neuroblatoma SH-SY5Y cells: 24h; GSE16766: Transcriptome analysis identifies molecular effectors of unconjugated bilirubin in human neuroblastoma SH-SY5Y cells: 1h; GSE16767: Transcriptome analysis identifies molecular effectors of unconjugated bilirubin in human neuroblastoma SH-SY5Y cells: 4h Experiment Overall Design: Refer to individual Series

2009-12-02 | E-GEOD-16768 | biostudies-arrayexpress

Gene expression profile in response to doxorubicin-rapamycin combined treatment of HER-2 overexpressing human mammary epithelial cell lines

Project description:HER-2 positive breast cancers frequently sustain elevated AKT/mammalian target rapamycin (mTOR) signaling which has been associated with resistance to doxorubicin treatment in the clinic. In our study we investigated if the mTOR inhibitor rapamycin increased the sensitivity to doxorubicin therapy in HB4a, a luminal normal mammary cell line; C5.2, a transformed cell derived from HB4a transfected with HER-2 and SKBR3 that exhibits HER-2 amplification. Flow cytometry analysis showed that the combination treatment for 24 hours with rapamycin 20nM and doxorubicin caused accumulation of HB4a and C5.2 cells in S-G2/M. Otherwise in SKBR3 cells, we observed a relative depletion of cells in S-G2/M and concomitant accumulation in G0/G1 of 10% of the cells. The analysis of IC50 of doxorubicin alone and in combination with rapamycin indicated that the sensitivity was increased 2.37 fold in HB4a, 2.46 in C5.2 and 1.87 in SKBR3, suggesting that rapamycin might have enhanced the effects of doxorubicin. Changes in gene expression resulting from co-treatment demonstrated that functional groups of genes with roles in cell cycle, proliferation, apoptosis regulation were represented in the 3 cells analysed. Other biological functions were exclusively associated with each cell suggesting that the inhibition of mTOR activation induced by HER-2 is complex and depends on the cellular context. Five independent experiments were performed for each treatment conditions: HB4a, C5.2 and SKBR3 cell lines were treated with vehicle (DRC), 20 nM of RAPAMYCIN alone (R) and 30 nM of DOXORUBICIN alone (D). The combined treatment consisted of 20 nM of RAPAMYCIN associated with 30 nM DOXORUBICIN of (DR). Total RNA extraction and hybridization on Affymetrix microarrays.

2011-01-13 | E-GEOD-26599 | biostudies-arrayexpress

Expression data from ARPE-19 cells treated with LDL or ox-LDL

Project description:LDL or Ox-LDL 200ug/ml, which showed no loss of viability after a 48 hour exposure, induced a physiological and pathological transcriptional response, respectively. LDL induced a downregulation of genes associated with cholesterol biosynthesis while ox-LDL induced transcriptional alterations in genes related to inflammation, matrix expansion, lipid metabolism and processing, and apoptosis. Pentraxin-3 was secreted into the culture medium after RPE cells were stimulated with ox-LDL, and immunohistochemically evident in Bruchs membrane of human macular samples with age-related macular degeneration. ARPE-19 cells exposed to 200ug/ml ox-LDL had a 38% apoptosis rate compared to less than 1% when exposed to LDL or untreated controls (p<0.0001). While LDL induced a physiologic response by RPE cells, a pathological phenotypic response was seen after treatment with oxidatively modified LDL. The transcriptional, biochemical, and functional data provide initial support of a role for the hypothesis that modified LDLs are one trigger for initiating events that contribute to the development of age-related macular degeneration. Keywords: treatment with non-treatment control Human ARPE-19 cells were exposed to LDL or oxidatively modified LDL (ox-LDL) for 48 hours for RNA extraction and hybridization on Affymetrix microarrays. We sought to determine whether retina, pigment epithelial cells develop a pathologic phenotype after exposure to low density lipoproteins (LDL) that are oxidatively modified.We have made two comparsions: LDL treatment versus non-treatment; ox-LDL treatment versus non-treatment.

2006-09-01 | E-GEOD-5741 | biostudies-arrayexpress

Effects of redox modulation by inhibition of Thioredoxin reductase on radiosensitivity and gene expression

Project description:The involvement the thioredoxin system in radiation resistance was investigated in human lung cancer cells by a combination of ionizing radiation and specific thioredoxin reductase-inhibition by a phosphine gold compound. Gene expression profiles (Human Gene 1.0 ST) of lung cancer cells subjected to ionizing radiation and/or inhibition of thioredoxin reductase were studied. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.

2010-12-03 | E-GEOD-25814 | biostudies-arrayexpress

Transcription profiling of human coronary artery endothelial cells treated with ADMA at 2uM (a pathophysiological dose) and 100uM (a pharmacological dose), for 24h

Project description:Asymmetric dimethylarginine (ADMA) is a naturally occurring inhibitor of nitric oxide synthesis that accumulates in wide range of diseases associated with endothelial dysfunction and enhanced atherosclerosis. Plasma ADMA has been implicated as a major novel cardiovascular risk factor, but the mechanisms by which low concentrations of ADMA produce adverse effects on the cardiovascular system are unclear. We have treated human coronary artery endothelial cells with ADMA at 2uM (a pathophysiological dose) and 100uM (a pharmacological dose), for 24h.

2005-09-01 | E-MEXP-377 | biostudies-arrayexpress

Transcription profiling of rat chondrocytes treated with glucosamine exogenous glucosamine globally protects chondrocytes from the arthritogenic effects of IL-1beta

Project description:Glucosamine proved to be a potent, broad-spectrum inhibitor of IL-1beta. Of the 2,813 genes whose transcription was altered by IL-1beta stimulation (p<0.0001), glucosamine significantly blocked the response in 2,055 (~73%). Glucosamine fully protected the chondrocytes from IL-1-induced expression of inflammatory cytokines, chemokines and growth factors as well as proteins involved in PGE2 and NO synthesis. It also blocked the IL-1-induced expression of matrix specific proteases such as MMPs -3,-9,-10,-12 and ADAMTS-1. Experiment Overall Design: Articular cartilage was isolated from the femoral heads of male Wistar rats under aseptic conditions. Chondrocytes were obtained by sequential digestion of the cartilage with pronase and type II collagenase. After filtration to remove tissue debris, the cells were cultured in 75-cm2 flasks in complete Dulbeccoâs Modified Eagle Medium (DMEM; supplemented with 10% fetal bovine serum and 1% penicillin-streptomycin at 37Â°C in a humidified atmosphere containing 5% CO2. Experiments were subsequently performed with second-passage cultures whereby the cells from the large cultures were trypsinized, pooled and seeded into twenty 25 cm2 flasks. These were then divided into 4 treatment groups to evaluate the effects of glucosamine and IL-1 on global transcription patterns.To the culture medium in half of the flasks, glucosamine, HCl was added to a final concentration of 20 mM. Six hours later, IL-1beta was added at 10 ng/ml to 5 of the flasks receiving glucosamine and to 5 of the untreated flasks. Fourteen hours post IL-1beta stimulation, total RNA was isolated individually from the respective cultures and microarray experiments processed.

2009-04-23 | E-GEOD-6119 | biostudies-arrayexpress

Transcription profiling of human neuroblastoma SH-SY5Y cells: 4h identifies molecular effectors of unconjugated bilirubin

Project description:The deposition of unconjugated bilirubin (UCB) in selected regions of the brain results in irreversible neuronal damage, or Bilirubin Encephalopathy (BE). Although UCB impairs a large number of cellular functions, the basic mechanisms of neurotoxicity have not yet been fully clarified. While cells can accumulate UCB by passive diffusion, cell protection may involve multiple mechanisms including the extrusion of the pigment as well as pro-survival homeostatic responses that are still unknown. The effects of UCB treatment to SH-SY5Y neuroblastoma cell line were examined by high-density oligonucleotide microarrays. 230 genes were induced after 24 hours. A Gene Ontology (GO) analysis showed that a large group of UCB-induced genes were components of the ER stress response. Independent experimental validation of molecular events crucial for the ER stress response is presented. The results show that UCB exposure induces the ER stress response as a major intracellular homeostatic response in neuroblastoma cells in vitro. Our finding may provide valuable information for new therapeutic strategies in the treatment of BE. Experiment Overall Design: We used high-density oligonucleotide microarrays to analyze the gene expression profile of human neuroblastoma SH-SY5Y cells upon UCB treatment. Three replicates of UCB-treated cells were analyzed. As controls, we used three replicates of the same cells treated with DMSO only (the solvent used for UCB treatment).

2009-12-02 | E-GEOD-16767 | biostudies-arrayexpress

Transcription profiling of human neuroblatoma SH-SY5Y cells: 24h identifies molecular effectors of unconjugated bilirubin

Project description:The deposition of unconjugated bilirubin (UCB) in selected regions of the brain results in irreversible neuronal damage, or Bilirubin Encephalopathy (BE). Although UCB impairs a large number of cellular functions, the basic mechanisms of neurotoxicity have not yet been fully clarified. While cells can accumulate UCB by passive diffusion, cell protection may involve multiple mechanisms including the extrusion of the pigment as well as pro-survival homeostatic responses that are still unknown. The effects of UCB treatment to SH-SY5Y neuroblastoma cell line were examined by high density oligonucleotide microarrays. 230 genes were induced after 24 hours. A Gene Ontology (GO) analysis showed that a large group of UCB-induced genes were components of the ER stress response. Independent experimental validation of molecular events crucial for the ER stress response is presented. The results show that UCB exposure induces ER stress response as major intracellular homeostatic response in neuroblastoma cells in vitro. Our finding may provide valuable information for new therapeutic strategies in the treatment of BE. Experiment Overall Design: We used high density oligonucleotide microarrays to analyze the gene expression profile of human neuroblastoma SH-SY5Y cells upon UCB treatment. Three replicates of UCB-treated cells were analyzed. As controls, we used three replicates of the same cells treated with DMSO only (the solvent used for UCB treatment).

2009-11-29 | E-GEOD-16656 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data