Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Azathioprine Antagonizes Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma

ABSTRACT: Azathioprine Antagonizes Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma

PROVIDER: PRJNA644511 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12134512_1.fastq.gz	Fastqsanger.gz
	SRR12134512_2.fastq.gz	Fastqsanger.gz
	SRR12134513_1.fastq.gz	Fastqsanger.gz
	SRR12134513_2.fastq.gz	Fastqsanger.gz
	SRR12162090_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [WES]

Project description:Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

2021-02-16 | GSE153680 | GEO

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [microarray]

Project description:Expression profiling of 559T(proneural subtype of glioblastoma), 592T(mesenchymal subtype of glioblastoma) and normal human astrocyte (NHA) Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate and temozolomide (TMZ) has been used as the standard chemotherapy for GBM treatment. However, a large number of patients either respond poorly to TMZ and/or develop resistance after long-term use, urging the need for the development of potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found azathioprine, an immunosuppressive medication, to be a promising therapeutic agent for TMZ-resistant GBM treatment. Through integrative genome-wide analysis and global proteomic analysis, we identified the elevated lipid metabolism due to hyperactive EGFR/AKT/SREBP-1 signaling pathway being inhibited by azathioprine. In addition, azathioprine causes ER stress-induced apoptosis. Orthotopic xenograft models injected with patient-derived GBM cells exhibits reduced tumor volumes and increased apoptosis by azathioprine. These overall data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

2021-02-16 | GSE153679 | GEO

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [RNA-Seq]

2021-02-16 | GSE153907 | GEO

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [WES]

Project description:Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [WES]

| PRJNA643683 | ENA

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [microarray]

Project description:Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [microarray]

| PRJNA643679 | ENA

Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [RNA-Seq]

Project description:Azathioprine Blocks the Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma [RNA-Seq]

| PRJNA644516 | ENA

Azathioprine antagonizes aberrantly elevated lipid metabolism and induces apoptosis in glioblastoma.

Project description:Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with poor survival rate. Temozolomide (TMZ) is used as standard chemotherapy to treat GBM, but a large number of patients either respond poorly and/or develop resistance after long-term use, emphasizing the need to develop potent drugs with novel mechanisms of action. Here, using high-throughput compound screening (HTS), we found that azathioprine, an immunosuppressant, is a promising therapeutic agent to treat TMZ-resistant GBM. Through integrative genome-wide analysis and global proteomic analysis, we found that elevated lipid metabolism likely due to hyperactive EGFR/AKT/SREBP-1 signaling was inhibited by azathioprine. Azathioprine also promoted ER stress-induced apoptosis. Analysis of orthotopic xenograft models injected with patient-derived GBM cells revealed reduced tumor volume and increased apoptosis after azathioprine and TMZ co-treatment. These data indicate that azathioprine could be a powerful therapeutic option for TMZ-resistant GBM patients.

| S-EPMC7957120 | biostudies-literature

Azathioprine Antagonizes Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-16 | GSE153908 | GEO

UCP1-dependent depletion of liver extracellular succinate antagonizes inflammatory pathogenesis

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver pathology worldwide and is intimately linked with obesity and type 2 diabetes. Liver inflammation is a hallmark of NAFLD and is thought to contribute to tissue fibrosis and disease pathogenesis. Uncoupling protein 1 (UCP1) is exclusively expressed in brown and beige adipocytes and has been extensively studied for its capacity to elevate thermogenesis and reverse obesity. Here we identify an endocrine pathway regulated by UCP1 that antagonizes liver inflammation and pathology, independent of effects on obesity. We show that, without UCP1, brown and beige fat exhibit a diminished capacity to clear succinate from the circulation. Moreover, UCP1KO mice exhibit elevated extracellular succinate in liver tissue that drives inflammation through ligation of its cognate receptor succinate receptor 1 (SUCNR1) in liver-resident stellate cell and macrophage populations. Conversely, increasing brown and beige adipocyte content in mice antagonizes SUCNR1-dependent inflammatory signaling in the liver. We show that this UCP1-succinate-SUCNR1 axis is necessary to regulate liver immune cell infiltration and pathology, and systemic glucose intolerance in an obesogenic environment. As such, the therapeutic utility of brown and beige adipocytes, and UCP1, extends beyond thermogenesis and may be leveraged to antagonize NAFLD and SUCNR1-dependent liver inflammation.

2022-02-17 | PXD024717 | Pride

Aberrantly microRNA profiling in cancerous hepatocytes versus normal primary hepatocytes

Project description:MicroRNAs is a rapidly expanding area expected to change the way in which diseases will be diagnosed, treated and monitored in the future. Hepatocellular carcinoma (HCC) shows a rising incidence with high mortality but lack of effective targeted therapies. We identified the aberrantly expressed miRNAs involved in HCC through the comparison of miRNA expression profiling in cancerous hepatocytes with that in normal primary human hepatocytes and found 37 dysregulated miRNAs in HCC. These aberrantly expressed miRNAs may provide insights into pathogenesis of HCC and thus may be used for diagnosis and therapy. Over the past few years, though several studies have uncovered aberrant miRNA expression profiles in HCC compared with matched nonmalignant tissues, the overlap of deregulated miRNAs from different platforms is limited. To solve this problem, we recommend a method that using primary cancer cells or cancer cell lines and nonmalignant primary cells to identify the specific aberrantly miRNA expression profiles in HCC and even in other types of cancer. Here, we identified the aberrantly expressed miRNAs involved in hepatoma through the comparison of miRNA expression profiling in cancerous hepatocytes with that in normal primary human hepatocytes and 37 dysregulated miRNAs were screened out by 2-fold change with a significant difference (P<0.05). Clustering analysis based on 13 miRNAs whose fold changes were over 15-fold change exhibited significantly differential expression pattern between the cancerous and normal hepatocytes.

2010-12-30 | E-GEOD-20077 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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