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Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: Gpd1 KO)

ABSTRACT: Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: Gpd1 KO)

PROVIDER: PRJNA434718 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6751100.fastq.gz	Fastqsanger.gz
	SRR6751110.fastq.gz	Fastqsanger.gz
	SRR6751101.fastq.gz	Fastqsanger.gz
	SRR6751111.fastq.gz	Fastqsanger.gz
	SRR6751102.fastq.gz	Fastqsanger.gz

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Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: Gpd1 KO)

Project description:Cancer stem cells (CSCs) are attractive targets for cancer therapy, however, little is known about how to target CSCs without affecting the normal stem cell population. Here we report the ribosome-profiling analysis of mouse neural stem cells and brain tumour stem cells (BTSCs), which leads to the identification of glycerol-3-phosphate dehydrogenase 1 (GPD1) as a CSC- specific determinant. We confirmed that GPD1 is expressed in BTSCs but not in neural stem cells. Intriguingly, expression of GPD1 is only found in the infiltrating dormant BTSCs in vivo and these cells start to divide and drive tumour relapse after chemotherapy. Most importantly, inhibition of GPD1 expression in tumour-bearing mice leads to prolonged survival. Further analysis shows that loss of GPD1 results in widespread changes in important pathways affecting BTSC maintenance. Human patient data analysis suggests that GPD1 is expressed in the dormant infiltrating tumour cells in human glioblastoma and the expression level is associated with a worse prognosis. This study provides an attractive therapeutic target for treating brain tumours and a novel aspect of regulation of CSC dormancy.

2019-07-15 | GSE110868 | GEO

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (Ribosome profiling)

2019-07-15 | GSE110866 | GEO

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma

Project description:Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma

| PRJNA434706 | ENA

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: NSC vs BTSC)

2019-07-15 | GSE110867 | GEO

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (Ribosome profiling)

Project description:Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (Ribosome profiling)

| PRJNA434716 | ENA

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: NSC vs BTSC)

Project description:Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma (RNA-seq: NSC vs BTSC)

| PRJNA434717 | ENA

Identification and validation of GPD1 as an essential cancer stem cell specific target in glioblastoma

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

2019-07-15 | GSE110869 | GEO

The FFPE samples of the primary vs. recurrent glioblastoma validation cohort

Project description:The FFPE samples of the primary vs. recurrent glioblastoma validation cohort

2022-08-08 | PXD035867 |

GPD1 enhances the anti-cancer effects of metformin by synergistically increasing total cellular glycerol-3-phosphate

Project description:GPD1 overexpression enhances the anti-cancer effect of metformin through synergistic inhibition of mitochondrial function, thereby providing new insight into metformin-mediated cancer therapy.

2020-03-15 | GSE146982 | GEO

Autophagy is essential for tumor development and survival in hypoxia and in vivo in glioblastoma. (Provisional)

Project description:Hypoxia is negatively associated with glioblastoma patient survival and contributes strongly to tumor resistance. Unfortunately novel anti-angiogenic therapy increases hypoxia and activates survival pathways in tumor cells leading to inevitable tumor relapse. Here we demonstrate that primary glioma cultures and cell lines depend on autophagy to survive severe hypoxia but also at normal oxygen levels. Positive regulators of autophagy are expressed at higher levels in tumor cells and induction in severe hypoxia is more prominent compared to normal brain cells. We demonstrate that autophagy is an essential/critical target for novel treatment in glioblastoma. We show ATG9A is induced by severe hypoxia and could be a novel player of the autophagic response in glioma cells. ATG9A targeting inhibited tumor growth, suggesting an essential role in glioma cell survival in vivo. While autophagy induction was also observed in normal astrocytes, glioma cells displayed a higher sensitivity towards autophagy inhibitors. Importantly, patient-derived cultures exhibited varying sensitivity towards anti-autophagy treatment, where certain cultures were dependent on autophagy already in normoxic conditions. The treatment of tumor bearing mice with the autophagy inhibitor chloroquine significantly increased mice survival, but combination treatment of the agent with bevacizumab did not reveal additive or synergistic effect. The present study demonstrates that inhibition of autophagy using chloroquine as a single agent provides a novel treatment strategy against glioblastoma. It remains to be seen whether autophagy inhibition will improve current standard of care treatment of newly diagnosed glioblastoma patients and whether more specific inhibitors will lead to stronger therapeutic outcome. (Provisional)

2015-11-10 | E-MTAB-3085 | biostudies-arrayexpress

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