ArticleMolecular neurobiology2024
Copper Homeostasis Based on Cuproptosis-Related Signature Optimizes Molecular Subtyping and Treatment of Glioma.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Integration of machine learning to develop a disulfidptosis model for predicting glioma prognosis, immunotherapy response, and drug.iScience · 2026Article
- Roles of cuproptosis in central nervous system tumors: from molecular mechanisms to therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
- Gut-Brain-Microbiome Axis in the Regulation of Cancer Immune Escape and Immunotherapy in Tumors.Research (Washington, D.C.) · 2025Review
- Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy.Biomarker research · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Copper is essential in living organisms and crucial to various physiological processes. Normal physiological conditions are in a state of copper homeostasis to ensure normal biochemical and metabolic processes. Dysregulation of copper homeostasis has been associated with multiple diseases, especially cancer. Cuproptosis is a copper-dependent cell death mediated by excess copper or homeostasis dysregulation. Elesclomol is a common inducer of cuproptosis, carrying copper into the cell and producing excess copper. Cuproptosis modulates tumor proliferation-related signaling pathways and is closely associated with remodeling the tumor microenvironment. In gliomas, the role of cuproptosis and copper homeostasis needs to be better characterized. This study systematically analyzed cuproptosis-related genes (CRGs) and constructed a cuproptosis signature for gliomas. The signature closely links the subtypes and clinical features of glioma patients. The results showed a greater tendency toward dysregulation of copper homeostasis as the malignant grade of glioma patients increased. In addition, CRGs-signature effectively predicted the sensitivity of glioma cells to elesclomol and verified that elesclomol inhibited glioma mainly through inducing cellular cuproptosis. In summary, we found different copper homeostatic features in gliomas and verified the anticancer mechanism of elesclomol, which provides a theoretical basis for developing novel therapeutic strategies for gliomas.
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Registered trials
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