ArticleNeuro-oncology2025
The proteomic landscape of diffuse midline glioma highlights the therapeutic potential of non-histone protein methyltransferases.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed.
- Targeting EHMT2 inhibition in glioblastoma: effects on tumor progression and STAT3 signaling.Translational cancer research · 2026Article
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Prognostic value of palmitoylation-regulated mechanisms in glioblastoma: integrated multi-omics analysis via least absolute shrinkage and selection operator (LASSO) regression and single-cell sequencing.Translational cancer research · 2026Article
- Adaptive immunotherapeutic paradigms in diffuse midline glioma: integrating epigenetic reprogramming, neuron-glioma interactions, and tumor microenvironment modulation.Journal of neuro-oncology · 2025Review
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Decoding the cancer cell proteome: A delicate equilibrium with the genome and epigenome.Neuro-oncology · 2025Article
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Abstract
backgroundDiffuse midline glioma (DMG) is a highly aggressive pediatric brain tumor with limited treatment options despite extensive genomic characterization. The aim of this study was to investigate the proteomic landscape of DMG to identify potential therapeutic targets.
methodsWe conducted a comprehensive proteomic analysis using LC-MS3, along with DNA methylation and DNA/RNA sequencing in 55 DMG patients' samples. post-translational modification profiling (phosphoproteome and methylproteome) was conducted in 30 patient samples. We then investigated the effects of modulating key protein targets on protein methylation, protein synthesis, and DMG cell growth in vitro and in vivo.
resultsDMGs exhibited high global protein methylation, with significant enrichment of translation machinery proteins and factors involved in apoptosis regulation. Surprisingly, while targets of key kinases were highly phosphorylated, overall protein phosphorylation was lower in DMG compared to normal brain tissues. Non-histone methyltransferases METTL13 and METTL21B, along with protein kinases PAK2, PRKACA, and AKT1, were identified as key players in DMG methylproteome and phosphoproteome, respectively. METTL13 knockdown led to reduced EEF1A1 protein methylation, a shift in oncoprotein synthesis, and inhibited DMG cell growth in vitro and in vivo.
conclusionsOur findings highlight the dependency of DMG on methyl-signaling pathways, particularly involving METTL13, which regulates EEF1A1 protein methylation and oncoprotein synthesis. Targeting the non-histone methyltransferases offers a promising therapeutic strategy for DMG. This study underscores the potential of post-translational modifications, specifically methyl-signaling pathways, as novel therapeutic targets for DMG and possibly other currently incurable cancers.
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