ArticleCell reports2024
Feedforward cysteine regulation maintains melanoma differentiation state and limits metastatic spread.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- MAPK Inhibitor-Tolerant Persister Cells in Melanoma: Mechanisms and Therapeutic Vulnerabilities.Cancer science · 2026Review
- Lipid droplet organized metabolic vulnerabilities in melanoma: from the MITF low state to ferroptosis sensitization.Frontiers in molecular biosciences · 2026Review
- Emerging Roles of Ferroptosis in Skin Pathophysiology.The Journal of investigative dermatology · 2025Review
- Lysosomal reduced thiols are essential for mouse embryonic development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Role of Solute Carriers in the Metabolic Reprogramming of Skin Diseases.Clinical reviews in allergy & immunology · 2025Review
- Preclinical study of microphthalmia-associated transcription factor inhibitor ML329 in gastrointestinal stromal tumor growth.Molecular therapy. Oncology · 2025Article
- JIP4 deficiency causes a lysosomal storage disease arising from impaired cystine efflux.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The inherent ability of melanoma cells to alter the differentiation-associated transcriptional repertoire to evade treatment and facilitate metastatic spread is well accepted and has been termed phenotypic switching. However, how these facets of cellular behavior are controlled remains largely elusive. Here, we show that cysteine availability, whether from lysosomes (CTNS-dependent) or exogenously derived (SLC7A11-dependent or as N-acetylcysteine), controls melanoma differentiation-associated pathways by acting on the melanocyte master regulator MITF. Functional data indicate that low cysteine availability reduces MITF levels and impairs lysosome functions, which affects tumor ferroptosis sensitivity but improves metastatic spread in vivo. Mechanistically, cysteine-restrictive conditions reduce acetyl-CoA levels to decrease p300-mediated H3K27 acetylation at the melanocyte-restricted MITF promoter, thus forming a cysteine feedforward regulation that controls MITF levels and downstream lysosome functions. These findings collectively suggest that cysteine homeostasis governs melanoma differentiation by maintaining MITF levels and lysosome functions, which protect against ferroptosis and limit metastatic spread.
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