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

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

PROVIDER: PRJNA434716 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6751080.fastq.gz	Fastqsanger.gz
	SRR6751081.fastq.gz	Fastqsanger.gz
	SRR6751082.fastq.gz	Fastqsanger.gz
	SRR6751073.fastq.gz	Fastqsanger.gz
	SRR6751074.fastq.gz	Fastqsanger.gz

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

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.

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

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

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

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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

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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)

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Elimination of dormant cancer stem cells by disrupting glucocorticoid mediated lipid metabolism in glioblastoma [treatment]

Project description:Little progress has been made in therapeutic treatment of glioblastoma (GBM) in the last decade despite rapid progress in molecular understanding of brain tumors. Targeting cancer stem cells was considered as a strategy to treat GBM. Here we show that the stress hormone glucocorticoid is essential for the maintenance of brain tumor stem cells (BTSCs), which are resistant to conventional therapy. The glucocorticoid receptor (GR) regulates metabolic plasticity and chemoresistance of the dormant BTSC via controlling expression of GPD1 (glycerol-3-phosphate dehydrogenase 1), which is an essential regulator of lipid metabolism in BTSCs. Genomic, lipidomic and cellular analysis confirm that GR/GPD1 regulation is essential for BTSCs metabolic plasticity and survival. We further demonstrate that the GR agonist dexamethasone (DEXA), which is commonly used to treat GBM edema, abolishes the effect of chemotherapy drug temozolomide (TMZ) by upregulating GPD1 and thus promoting tumor cell dormancy and TMZ resistance, this provides a mechanistic explanation and thus settle the debate of steroid usage in brain tumor patient edema control. Pharmacological inhibition of GR/GPD1 pathway disrupts metabolic plasticity, induces ferroptosis and immune activation thus prolongs animal survival, which is superior to standard chemotherapy. This study identifies an important mechanism regulating cancer stem cell dormancy and provides a new opportunity for GBM treatment.

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Elimination of dormant cancer stem cells by disrupting glucocorticoid mediated lipid metabolism in glioblastoma [shRNA KD]

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