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Gene expression profile of Idh1 wild-type and mutant glioma initiating cells

ABSTRACT: Gene expression profile of Idh1 wild-type and mutant glioma initiating cells

PROVIDER: PRJNA490170 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7814792_1.fastq.gz	Fastqsanger.gz
	SRR7814792_2.fastq.gz	Fastqsanger.gz
	SRR7814793_1.fastq.gz	Fastqsanger.gz
	SRR7814793_2.fastq.gz	Fastqsanger.gz
	SRR7814794_1.fastq.gz	Fastqsanger.gz

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Project description:Isocitrate dehydrogenase 1 (IDH1) mutations are key drivers of glioma biology, influenc-ing tumor aggressiveness and treatment response. To elucidate their molecular impact, we performed proteome analysis on patient-derived (PD) and U87MG glioma cell models with either mutant or wildtype IDH1. We quantified over 6,000 protein groups per model, identifying 1,594 differentially expressed proteins in PD-AS (IDH1MUT) vs. PD-GB (IDH1WT) and 904 in U87MUT vs. U87WT. Both IDH1MUT models exhibited enhanced MHC antigen presentation and interferon signaling, indicative of an altered immune microen-vironment. However, metabolic alterations were model-dependent: PD-AS cells shifted toward glycolysis and purine salvage, while U87MUT cells retained oxidative phosphory-lation, potentially due to D2-hydroxyglutarate (2OHG)-mediated HIF1A stabilization. We also observed a predominance of downregulated DNA repair proteins in IDH1MUT mod-els, particularly those involved in homologous recombination. In contrast, RB1 and AS-MTL were strongly upregulated in both IDH1MUT models, implicating them in DNA repair and cellular stress responses. We also found distinct expression patterns of proteins reg-ulating histone methylation in IDH1MUT cells, favoring increased methylation of H3K4, H3K9, and H3K36. A key driver of this may be the upregulation of SETD2 in PD-AS, an H3K4 and H3K36 trimethyltransferase linked to recruitment of HIF1A as well as DNA mismatch repair proteins. This study uncovers candidate biomarkers and pathways rele-vant to glioma progression and therapeutic targeting but also underscores the complexity of predicting glioma pathogenesis and treatment responses based on IDH1 mutation sta-tus. While proteome profiling provides valuable insights, a comprehensive understand-ing of IDH1MUT gliomas will likely require integrative multi-omics approaches, including DNA/RNA methylation profiling, histone and protein post-translational modification analyses, and targeted DNA damage and repair assays.

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Gene expression profile of Idh1 wild-type and mutant glioma initiating cells

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