ArticleNeuro-oncology2026
Cysteine addiction in drug resistant glioblastoma and therapeutic targeting with designer selenium compounds.
Article in Neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- E3 ligase LMO7 promotes ALKBH2 ubiquitination to sensitize MGMT-deficient glioblastoma to temozolomide.Cell death & disease · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
backgroundCysteine is a multifunctional amino acid that can be oxidized affecting disulfide bond formation, redox signaling, and protein function. Reactive oxygen species (ROS) and the metabolic environment dictate cysteine uptake and oxidation status-especially in redox sensitive pathways. As many chemotherapeutic agents increase ROS, including the standard care for glioblastoma (GBM), temozolomide (TMZ), we hypothesized that TMZ-resistant (TMZ-R) GBM would have increased ROS affecting cysteine reactivity that could be therapeutically targeted.
methodsHere, to study the metabolic state within drug sensitive and resistant GBM, we used metabolite tracing with13 C-Cyst(e)ine, specialized cysteine reactivity proteomics and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) screening with drug treatments to determine the efficacy of targeting cysteine metabolic pathways with our designer selenium drug in both patient-derived cell lines and patient-derived xenograft GBM -orthotopic models.
resultsWe show that TMZ-R have increased cyst(e)ine uptake, cysteine reactivity, and sensitivity to selenium (Se)-containing compounds-which can bind cysteine-in vitro and in vivo. We show that in TMZ-R models selenium compound treatment increases the need for thioredoxin reductases where co-treatment of Se compounds and the thioredoxin inhibitor auranofin significantly improves overall survival in mouse models.
conclusionsOverall, our findings show a unique metabolic environment in TMZ-R models where designer brain penetrant Se-containing compounds target cysteine reactivity within proteins necessary for cancer cell survival and hold therapeutic potential.
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