ArticleNature metabolism2025
D-cysteine impairs tumour growth by inhibiting cysteine desulfurase NFS1.
Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Cysteine excess triggers a mitochondrial iron-dependent cell death.Nature metabolism · 2026Article
- The high price of 'free' cysteine.Nature metabolism · 2026Article
- Triple-Microenvironment Decoding Enables Logic-Unlocked Precision Photoimmunotherapy.Angewandte Chemie (International ed. in English) · 2026Article
- Integrated transcriptomic and in silico structural analysis identifies NFS1 and HSPA9 as potential regulators associated with mitochondrial ferroptosis and cell death resistance in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The iron-sulfur cluster assembly factor FDX2 is required for tumor initiation but not for growth of established tumors in transplantation models.The Journal of biological chemistry · 2026Article
- NFS1 Plays a Critical Role in Regulating Ferroptosis Homeostasis.Biomolecules · 2025Review
- Structural insights into the Urm1-Uba4 pathway and its biological roles.Essays in biochemistry · 2025Review
- Narciclasine as a Novel Treatment for Lung Cancer and Malignant Pleural Mesothelioma: Insights from 3D Tumor Spheroid Models.International journal of molecular sciences · 2025Article
- D-cysteine impairs tumour growth by inhibiting cysteine desulfurase NFS1.Nature metabolism · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Selective targeting of cancer cells is a major challenge for cancer therapy. Many cancer cells overexpress the cystine/glutamate antiporter xCT/CD98, an L-cystine transport system that strengthens antioxidant defences, thereby promoting tumour survival and progression. Here, we show that the D-enantiomer of cysteine (D-Cys) is selectively imported into xCT/CD98-overexpressing cancer cell lines and impairs their proliferation, particularly under high oxygen concentrations. Intracellular D-Cys specifically inhibits the mitochondrial cysteine desulfurase NFS1, a key enzyme of cellular iron-sulfur protein biogenesis, by blocking sulfur mobilization due to steric constraints. NFS1 inhibition by D-Cys affects all cellular iron-sulfur cluster-dependent functions, including mitochondrial respiration, nucleotide metabolism and maintenance of genome integrity, leading to decreased oxygen consumption, DNA damage and cell cycle arrest. D-Cys administration diminishes tumour growth of human triple-negative breast cancer cells implanted orthotopically into the mouse mammary gland. Hence, D-Cys could represent a simple therapy to selectively target those forms of cancer characterized by overexpression of xCT/CD98.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.