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Dimethyl alpha-ketoglutarate inhibits proliferation in diffuse intrinsic pontine glioma by reprogramming epigenetic and transcriptional networks

ABSTRACT: Dimethyl alpha-ketoglutarate inhibits proliferation in diffuse intrinsic pontine glioma by reprogramming epigenetic and transcriptional networks

PROVIDER: PRJNA993407 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25223732_1.fastq.gz	Fastqsanger.gz
	SRR25223732_2.fastq.gz	Fastqsanger.gz
	SRR25223733_1.fastq.gz	Fastqsanger.gz
	SRR25223733_2.fastq.gz	Fastqsanger.gz
	SRR25223734_1.fastq.gz	Fastqsanger.gz

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Dimethyl alpha-ketoglutarate inhibits proliferation in diffuse intrinsic pontine glioma by reprogramming epigenetic and transcriptional networks

Project description:Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brain tumor with limited therapeutic options. Here, we investigated the potential of dimethyl alpha-ketoglutarate (DMKG) as an anti-proliferative agent against DIPG and unraveled its underlying molecular mechanisms. DMKG exhibited robust inhibition of DIPG cell proliferation, colony formation, and neurosphere growth. Transcriptomic analysis revealed substantial alterations in gene expression, with upregulated genes enriched in hypoxia-related pathways and downregulated genes associated with cell division and the mitotic cell cycle. Notably, DMKG induced G1/S phase cell cycle arrest and downregulated histone H3 lysine 27 acetylation (H3K27ac) without affecting H3 methylation levels. The inhibition of AKT and ERK signaling pathways by DMKG coincided with decreased expression of the CBP/p300 coactivator. Importantly, we identified the c-MYC-p300/ATF1-p300 axis as a key mediator of DMKG's effects, demonstrating reduced binding to target gene promoters and decreased H3K27ac levels. Depletion of c-MYC or ATF1 effectively inhibited DIPG cell growth. These findings highlight the potent anti-proliferative properties of DMKG, its impact on epigenetic modifications, and the involvement of the c-MYC-p300/ATF1-p300 axis in DIPG, shedding light on potential therapeutic strategies for this devastating disease.

2023-10-26 | GSE237008 | GEO

Wnt5a and its downstream transcription factor Stat3 are therapeutic targets for diffuse intrinsic pontine gliomas

Project description:Understand how Wnt5a depletion affects the growth of diffuse intrinsic pontine gliomas

2019-04-29 | GSE130407 | GEO

Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

Project description:Purpose: More than 90% of children with diffuse intrinsic pontine glioma (DIPG) die within 2 years of diagnosis. There is a dire need to identify therapeutic targets, however lack of patient material for research has limited progress. We evaluated a large cohort of diffuse intrinsic pontine gliomas (DIPGs) to identify recurrent genomic abnormalities and gene expression signatures underlying DIPG. Patients and Methods: We used single nucleotide polymorphism arrays to evaluate genomic copy number imbalances in 43 DIPGs from 40 patients and in 8 low-grade exophytic brainstem gliomas. Gene expression arrays were used to evaluate expression signatures from 27 DIPGs, 6 low-grade exophytic brainstem gliomas and 66 low-grade gliomas arising outside the brainstem. Results: Frequencies of specific large-scale and focal imbalances varied significantly between DIPGs and pediatric glioblastomas outside the brainstem. Focal amplifications of genes within the receptor tyrosine kinase-Ras-PI3-kinase signaling pathway were found in 47% of DIPG, with PDGFRA and MET showing the highest frequency. 30% of DIPG contained focal amplifications of cell-cycle regulatory genes controlling RB phosphorylation, and 21% had concurrent amplification of genes from both pathways. Some tumors showed heterogeneity in amplification patterns. DIPGs showed distinct gene expression signatures relating to developmental processes compared to pediatric glioblastomas arising outside the brainstem, while expression signatures of low-grade exophytic brainstem gliomas were similar to low-grade gliomas outside the brainstem. Copy number analaysis: 43 DIPG samples, 8 Low Grade Gliomas using SNP6.0. Available matched normals are also profiled with SNP6.0. Expression analysis: 29 DIPG samples, 6 Low grade samples Please contact Suzanne Baker at Suzanne.Baker@stjude.org for CEL files and genotype calls.

2011-09-20 | E-GEOD-26576 | biostudies-arrayexpress

Circulating microRNA profiling in diffuse intrinsic pontine gliomas

Project description:Circulating microRNA profiling in diffuse intrinsic pontine gliomas

| PRJNA672708 | ENA

Circulating microRNA profiling in diffuse intrinsic pontine gliomas

Project description:Diffuse midline glioma (DMG) identifies gliomas originating in the thalami, brainstem, cerebellum and spine. Within this entity, tumours that infiltrate the pons, called diffuse intrinsic pontine gliomas (DIPGs), have a rapid onset and devastating neurological symptoms. Radiotherapy is the only intervention that is able to modify the disease course, albeit not in a curative way. In recent years, liquid biopsies have represented the next step in clinical diagnostics due to their easily accessible nature. The purpose of this study is to profile circulating miRNA expression to disclose a potential prognostic signature with clinical impact.

2022-12-21 | GSE160249 | GEO

Next Generation Sequencing of Diffuse Intrinsic Pontine Glioma Samples

Project description:Next Generation Sequencing of Diffuse Intrinsic Pontine Glioma Samples

| PRJNA431328 | ENA

Next Generation Sequencing of Diffuse Intrinsic Pontine Glioma Samples

Project description:Next Generation Sequencing of Diffuse Intrinsic Pontine Glioma Samples

| PRJNA431329 | ENA

Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

2011-09-21 | GSE26576 | GEO

Utilizing Omomyc to Target MYCN-Amplified Diffuse Intrinsic Pontine Gliomas

Project description:Utilizing Omomyc to Target MYCN-Amplified Diffuse Intrinsic Pontine Gliomas

| PRJNA833664 | ENA