Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of DGAT knockdown on gene expression in A498 xenograft tumors

ABSTRACT: The metabolic enzyme diglyceride acyltransferase (DGAT) is responsible for the synthesis of triglycerides. Loss of its expression may sensitize cells to conditions of nutrient and oxygen that are commonly present in tumors. This study is designed to identify stress response pathways that may be induced following the shRNA-mediated knockdown of the two genes coding for the DGAT enzymes. We used microarrays to detail the global programme of gene expression following DGAT knockdown in vivo and identified differentially regulated gene sets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE117774 | GEO | 2018/07/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of DGAT loss on hypoxic tumor cells growing under serum-deprived conditions

Project description:The metabolic enzyme diglyceride acyltransferase (DGAT) is responsible for the synthesis of triglycerides. Loss of its expression may sensitize cells to conditions of nutrient and oxygen that are commonly present in tumors. This study is designed to identify stress response pathways that may be induced following the shRNA-mediated knockdown of the two genes coding for the DGAT enzymes. In vitro growth conditions lacking serum and oxygen were used to mimic growth conditions commonly found in poorly perfused tumor domains We used a microarray study to identify global transcriptional changes in kidney cancer cells (A498) grown under serum deprived conditions. DGAT was knocked down using doxycycline, which induced DGAT1/2 shRNA expression. The effects of both DGAT loss and oxygen deprivation on the transcriptome were tested.

2018-07-28 | GSE117775 | GEO

Effect of DGAT knockdown on gene expression in A498 xenograft tumors

Project description:Effect of DGAT knockdown on gene expression in A498 xenograft tumors

| PRJNA483167 | ENA

GFP and mCherry gene expression at single cell level of all liver cell types from B6J mice

Project description:Diacylglycerol acyltransferase (DGAT)-2 catalyzes the final step of triglyceride (TG) synthesis. DGAT2 deletion in mice lowers liver TGs and DGAT2 overexpression might have the opposite effect. Mouse DGAT2 was overexpressed in C57Bl/6J mice using adeno-associated virus 8 (AAV8 and AAV-DJ). The tissue specificity of AAV8 and AAV-DJ was first evaluated. To confirm that AAV8 and AAV-DJ only infected hepatocytes and not other cells in liver, we carried out single cell sequencing of liver cells isolated from mice infected with AAV8-mCherry and AAV-DJ-GFP. The mCherry and GFP signals were highly expressed in hepatocytes and not in stellate, endothelial, or Kupffer cells.

2024-01-30 | GSE250338 | GEO

Hepatocyte Deletion of Triglyceride-Synthesis Enzyme DGAT2 Reduces Steatosis without Increasing Inflammation or Fibrosis

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by excess lipid accumulation in hepatocytes and reprepresents a huge public health problem owing to its propensity to progress to non-alcoholic steatohepatitis (NASH), fibrosis, and liver failure. The lipids stored in hepatic steatosis are primarily triglycerides (TGs) synthesized by two acyl CoA:diacylglycerol acyltransferase (DGAT) enzymes. Either DGAT1 or DGAT2 catalyzes this reaction, and these enzymes have been suggested to differentially utilize exogenous or endogenously synthesized fatty acids, with DGAT2 being linked to storage of fatty acids from de novo lipogenesis, a process that is increased in NAFLD. However, whether DGAT2 is more responsible for lipid accumulation in NAFLD and the progression to fibrosis is currently unknown. Also, it is unresolved whether DGAT2 can be safely inhibited as a therapy for NAFLD. Here we induced NAFLD-like disease in mice by feeding a diet rich in fructose, saturated fat, and cholesterol and found that hepatocyte-specfici Dgat2 deficiency reduced expression of de novo lipogenesis genes and lowered liver TGs by ~70%. Importantly, the reduction of steatosis was not accompanied by increased inflammation or fibrosis, and insulin and glucose metabolism were unchanged. Conclusion: This study suggests that hepatic DGAT2 deficiency successfully reduced diet-induced hepatic steatosis and supports the development of DGAT2 inhibitors as a therapeutic strategy for treating NAFLD and preventing downstream consequences.

2020-05-26 | PXD013423 | Pride

Expression data from HCT116 cells following CTNNB1 knockdown

Project description:We used microarrays to detail the global programme of gene expression following CTNNB1 knockdown in HCT116 cells

2016-09-29 | GSE87429 | GEO

Expression data from HCT116 cells following CDK8 knockdown

Project description:We used microarrays to detail the global programme of gene expression following CDK8 knockdown in HCT116 cells

2016-09-29 | GSE87428 | GEO

Expression data from HCT116 cells following H19 knockdown

Project description:Knockdown of H19 leads to cell cycle arrest, reduced cell proliferation, and reduced cell migration in HCT116 cells. We used microarrays to detail the global programme of gene expression following H19 knockdown in HCT116 cells

2016-09-29 | GSE87430 | GEO

Expression data from DLD1 cells following H19 knockdown

Project description:Knockdown of H19 leads to cell cycle arrest, reduced cell proliferation, and reduced cell migration in DLD1 cells. We used microarrays to detail the global programme of gene expression following H19 knockdown in DLD1 cells

2016-09-29 | GSE87427 | GEO

A specific lipid metabolic profile is associated with the epithelial mesenchymal transition program

Project description:Several studies have identified a specific metabolic program that is associated with the process of epithelial-mesenchymal transition (EMT). Whereas much is known about the association between glucose metabolism and EMT, the contribution of lipid metabolism is not still completely understood. Here, we studied epithelial and mesenchymal breast cancer cells by proteomic and lipidomic approaches and identified significant differences that characterised these models concerning specific metabolic enzymes and metabolites including fatty acids and phospholipids. Higher levels of monounsaturated fatty acids together with increased expression of enzymes of de novo fatty acid synthesis is the distinct signature of epithelial with respect to mesenchymal cells that, on the contrary, show reduced lipogenesis, higher polyunsaturated fatty acids level and increased expression of genes involved in the triglyceride (TAG) synthesis and lipid droplets formation. In the mesenchymal model, the diacylglycerol acyltransferase (DGAT)-1 appears to be the major enzyme involved in TAG synthesis and inhibition of DGAT1, but not DGAT2, drastically reduces the incorporation of labeled palmitate into TAG. Moreover, knockdown of β-catenin demonstrated that this metabolic phenotype in under the control of a network of transcriptional factors and that β-catenin has a specific role in the regulation of lipid metabolism in mesenchymal cells.

2019-01-02 | PXD011854 | Pride

The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis through inhibition of Wnt signaling

Project description:The developmental transcription factor SOX6 was found to regulate serum, as well as liver triglycerides in BL6 mice treated with SOX6 antisense gapmers compared to control gapmers. SOX6 was initially discovered as a gene over-expressed in mesenchymal stem cells derived from small for gestational age newborns. We characterized its metabolic function in BL6 mice using the above antisense knockdown approach. BL6 mice were treated with either SOX6 specific or control gapmer oligonucleotides for 48h. Knockdown efficiency was measured in liver and epididymal white adipose tissues and serum levels of triglycerides and cholesterol quantified.

2015-06-26 | E-GEOD-70300 | 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