ArticleThe Journal of biological chemistry2025
Methionine cycle inhibition disrupts antioxidant metabolism and reduces glioblastoma cell survival.
Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Integrative proteomics and metabolomics advance early cancer detection and targeted therapy with emerging technologies and clinical applications.Discover oncology · 2026Review
- AHCY: A metabolic gatekeeper at the interface of methylation, redox balance, and cellular stress response.The Journal of biological chemistry · 2026Review
- Bioinformatics identification of adenosylhomocysteinase (AHCY) as a regulator of ferroptosis in nasopharyngeal carcinoma cells via the Hippo-Yes-associated protein (Hippo-YAP) pathway.Translational cancer research · 2026Article
- Multi-omics characterization identifies AHCY as a prognostic biomarker driving immunometabolic reprogramming in bladder cancer.Translational oncology · 2026Article
- The Methionine-Mitochondria Axis in Cancer: Metabolic Cross-Talk and Therapeutic Vulnerabilities.Current pharmacology reports · 2026Review
- Integrated bulk and single-cell transcriptomics unveil the role of AHCY in cell cycle regulation of endometrial cancer.Frontiers in oncology · 2026Article
- Article
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- Article
- IDENTIFICATION OF DISEASE-SPECIFIC VULNERABILITY STATES AT THE SINGLE-CELL LEVEL.bioRxiv : the preprint server for biology · 2025Article
- Quercetin promotes production of secondary hair follicle stem cells in cashmere goat: a mechanistic study.Frontiers in veterinary science · 2025Article
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4 authors.
Funding
Abstract
Glioblastoma (GBM) is a highly aggressive primary malignant adult brain tumor that inevitably recurs with a fatal prognosis. This is due in part to metabolic reprogramming that allows tumors to evade treatment. Therefore, we must uncover the pathways mediating these adaptations to develop novel and effective treatments. We searched for genes that are essential in GBM cells as measured by a whole-genome pan-cancer CRISPR screen available from DepMap and identified the methionine metabolism genes MAT2A and AHCY. We conducted genetic knockdown, evaluated mitochondrial respiration, and performed targeted metabolomics to study the function of these genes in GBM. We demonstrate that MAT2A or AHCY knockdown induces oxidative stress, hinders cellular respiration, and reduces the survival of GBM cells. Furthermore, selective MAT2a or AHCY inhibition reduces GBM cell viability, impairs oxidative metabolism, and shifts the cellular metabolic profile towards oxidative stress and cell death. Mechanistically, MAT2a and AHCY regulate spare respiratory capacity, the redox buffer cystathionine, lipid and amino acid metabolism, and prevent oxidative damage in GBM cells. Our results point to the methionine metabolic pathway as a novel vulnerability point in GBM.
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