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Isocitrate Dehydrogenase 1 Primes Group-3 Medulloblastomas For Cuproptosis

ABSTRACT: Isocitrate Dehydrogenase 1 Primes Group-3 Medulloblastomas For Cuproptosis

PROVIDER: PRJNA1169346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30893478_1.fastq.gz	Fastqsanger.gz
	SRR30893478_2.fastq.gz	Fastqsanger.gz
	SRR30893479_1.fastq.gz	Fastqsanger.gz
	SRR30893479_2.fastq.gz	Fastqsanger.gz
	SRR30893480_1.fastq.gz	Fastqsanger.gz

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Isocitrate Dehydrogenase 1 Primes Group-3 Medulloblastomas For Cuproptosis

Project description:MYC-driven Group-3 medulloblastomas (MB) are malignant pediatric brain cancers without cures. To define actionable metabolic dependencies, we identified upregulationof dihydrolipoyl transacetylase (DLAT), the E2-subunit of pyruvate dehydrogenasecomplex (PDC) in a subset of Group-3 MB with poor prognosis. DLAT was induced by c-MYC and targeting DLAT lowered TCA-cycle metabolism and glutathione synthesis in Group-3 MB cells. We also noted upregulation of isocitrate dehydrogenase 1 (IDH1) in Group-3 MB. Remarkably, genetic and pharmacologic suppression of IDH1 epigenetically reduced c-MYC and downstream DLAT levels. DLAT is a central regulator of cuproptosis, a copper-dependent cell death mechanism induced by the copper ionophore elesclomol. DLAT expression in Group-3 MB cells correlated with increased sensitivity to cuproptosis. Elesclomol was CNS-penetrant and suppressed tumor growth in vivo in Group-3 MB animal models. Our data uncover an IDH1/c-MYC dependent vulnerability that regulates DLAT levels and can be targeted to kill Group-3MB by cuproptosis.

2025-04-10 | GSE278880 | GEO

Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of myeloid and lymphoid cell type diversity with our m-RNA sequencing interrogation.

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

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Hepatic transcriptomics reveals that lipogenesis is a key signaling pathway in isocitrate dehydrogenase 2 deficient mice

Project description:The present study was conducted to capture signatures of isocitrate dehydrogenase 2 deficient (Idh2-/-) mice liver transcriptome using mRNA sequencing technique which provides information to discover new transcripts and to quantify transcript levels. Using this mRNA sequencing results, bioinformatic analyses will be performed to further identify key biological functions of Idh2 influencing disease-related signaling pathways.

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Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of T cells from brain TIME at single cell resolution, which served as part of our pan-cancer T cell atlas analysis.

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Project description:Cuproptosis is characterized by the aggregation of lipoylated components of the tricarboxylic acid cycle and subsequent loss of iron-sulfur cluster proteins as a unique copper-dependent form of regulated cell death. Dysregulation of copper homeostasis and resulting cuproptosis induction is an emerging area of interest for cancer therapy. However, mechanisms of cancer cell evasion of cuproptosis are not well understood. Here, we found that the cuproptosis process is accompanied by activation of the Wnt/β-catenin pathway. Mechanistically, copper binds to PDK1 and promotes its interaction with AKT, resulting in activation of the Wnt/β-catenin pathway and cancer stem cell (CSC) properties. Notably, aberrant activation of Wnt/β-catenin signaling conferred resistance of CSCs to cuproptosis. Further studies showed that the β-catenin/TCF4 transcriptional complex directly binds to the promoter region of ATP7B, a protein responsible for the efflux of copper ions from the cell, inducing its expression and reducing intracellular copper accumulation, thereby inhibiting cuproptosis. Knockdown of TCF4 or pharmacological blockade of the Wnt/β-catenin pathway increased the sensitivity of CSCs to elesclomol-Cu-induced cuproptosis. These findings reveal a link between copper homeostasis regulated by the Wnt/β-catenin pathway and cuproptosis sensitivity, and may provide a precision medicine strategy for cancer treatment by selectively inducing cuproptosis

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