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

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

PROVIDER: PRJNA644516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12162090_1.fastq.gz	Fastqsanger.gz
	SRR12162090_2.fastq.gz	Fastqsanger.gz
	SRR12162091_1.fastq.gz	Fastqsanger.gz
	SRR12162091_2.fastq.gz	Fastqsanger.gz
	SRR12162092_1.fastq.gz	Fastqsanger.gz

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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]

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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 Antagonizes Aberrantly Elevated Lipid Metabolism and Induces Apoptosis in Glioblastoma

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

| PRJNA644511 | 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

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

denitrification and elevated temperature

Project description:denitrification and elevated temperature

| PRJEB55872 | ENA