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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma. [CRISPRseq]

ABSTRACT: Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma. [CRISPRseq]

PROVIDER: PRJNA887789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21831653.fastq.gz	Fastqsanger.gz
	SRR21831654.fastq.gz	Fastqsanger.gz
	SRR21831655.fastq.gz	Fastqsanger.gz
	SRR21831656.fastq.gz	Fastqsanger.gz

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma

Project description:Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma. [CRISPRseq]

Project description:MYC-driven medulloblastoma (MB) is an aggressive pediatric brain tumor characterized by therapy resistance and disease recurrence. Here we integrated data from unbiased genetic screening and metabolomic profiling to identify multiple cancer-selective metabolic vulnerabilities in MYC-driven MB tumor cells, which are amenable to therapeutic targeting. Among these targets, dihydroorotate dehydrogenase (DHODH), an enzyme that catalyzes de novo pyrimidine biosynthesis, emerged as a favorable candidate for therapeutic targeting. Mechanistically, DHODH inhibition acts on-target leading to uridine metabolite scarcity and hyperlipidemia, accompanied by reduced protein O-GlcNAcylation and c-Myc degradation. Pyrimidine starvation evokes a metabolic stress response that leads to cell cycle arrest and apoptosis. We further show that an orally available small molecule DHODH inhibitor demonstrates potent mono-therapeutic efficacy against patient-derived MB xenografts in vivo. The reprogramming of pyrimidine metabolism in MYC-driven medulloblastoma represents an unappreciated therapeutic strategy and a potential new class of treatments with stronger cancer selectivity and fewer neurotoxic sequelae.

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [EPIC]

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [RNA-seq]

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [EPIC]

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [RNA-seq]

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Proteomic research on effect of EIF4A1 inhibition in MYC-amplified Group 3 medulloblastoma

Project description:As the most life-threatening subtype of pediatric medulloblastoma (MB), MYC-amplified Group 3 (G3) MB lacks effective and selective therapeutics. We tried to indirectly target MYC (oncogenic driver and cancer-dependent molecule) production via inhibiting translational machinery. Through multiple datasets analyses on components of eIF4F (eukaryotic translation initiation factor 4F) complex, we found that EIF4A1 (major component with RNA helicase activity) has relatively higher expression level and the closest positive correlation with MYC in G3-MB among normal control and other 3 subtypes (e.g., WNT, SHH and G4). Both in vitro and in vivo experiments with MYC-amplified G3-MB cell lines showed effective growth inhibition upon EIF4A1 knockout or inhibitor treatment. Further FACS analysis found decreased cell proliferation and enhanced apoptosis on EIF4A1 inhibitor treatment. To explore the mechanisms of EIF4A1 inhibition on arresting MYC-amplified G3-MB, we performed the whole proteome analyses on corresponding MB cells treated with EIF4A1 inhibitor.

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Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma

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

2022-11-09 | GSE214803 | GEO

A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

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A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

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