ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013
Frequent inactivation of cysteine dioxygenase type 1 contributes to survival of breast cancer cells and resistance to anthracyclines.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 88 citations in OpenAlex.
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- Hepatocyte and adipocyte CDO1-mediated intracellular cysteine catabolism differentially modulates diet-induced obesity and fatty liver in mice.bioRxiv : the preprint server for biology · 2025Article
- Exploring the Role of CDO1 in Breast Cancer: Insights into Tumor Biology and Therapeutic Potential.Annals of surgical oncology · 2025Article
- Ferroptosis and its role in gastric and colorectal cancers.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Review
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- Deletion of hepatocyte cysteine dioxygenase type 1, a bile acid repressed gene, enhances glutathione synthesis and ameliorates acetaminophen hepatotoxicity.Biochemical pharmacology · 2024Article
- A Nonheme Iron(III) Superoxide Complex Leads to Sulfur Oxygenation.Journal of the American Chemical Society · 2024Article
- Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis ineLife · 2024Article
- Ferroptosis is Involved in the Pharmacological Effect of Ginsenoside.Mini reviews in medicinal chemistry · 2024Review
- Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis inbioRxiv : the preprint server for biology · 2023Article
- The transcription factor HBP1 promotes ferroptosis in tumor cells by regulating the UHRF1-CDO1 axis.PLoS biology · 2023Article
- Cysteine dioxygenase type 1 (CDO1): Its functional role in physiological and pathophysiological processes.Genes & diseases · 2023Review
- Cysteine dioxygenase 1 attenuates the proliferation via inducing oxidative stress and integrated stress response in gastric cancer cells.Cell death discovery · 2022Article
- Electronic Structure and Reactivity of Dioxygen-Derived Aliphatic Thiolate-Ligated Fe-Peroxo and Fe(IV) Oxo Compounds.Journal of the American Chemical Society · 2022Article
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- Induction and application of ferroptosis in cancer therapy.Cancer cell international · 2022Review
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Corrections and comments
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Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
Abstract
purposeGenome-wide DNA methylation analyses have identified hundreds of candidate DNA-hypermethylated genes in cancer. Comprehensive functional analyses provide an understanding of the biologic significance of this vast amount of DNA methylation data that may allow the determination of key epigenetic events associated with tumorigenesis. EXPERIMENTAL
designTo study mechanisms of cysteine dioxygenase type 1 (CDO1) inactivation and its functional significance in breast cancer in a comprehensive manner, we screened for DNA methylation and gene mutations in primary breast cancers and analyzed growth, survival, and reactive oxygen species (ROS) production in breast cancer cells with restored CDO1 function in the context of anthracycline treatment.
resultsDNA methylation-associated silencing of CDO1 in breast cancer is frequent (60%), cancer specific, and correlates with disease progression and outcome. CDO1 function can alternatively be silenced by repressive chromatin, and we describe protein-damaging missense mutations in 7% of tumors without DNA methylation. Restoration of CDO1 function in breast cancer cells increases levels of ROS and leads to reduced viability and growth, as well as sensitization to anthracycline treatment. Priming with 5-azacytidine of breast cancer cells with epigenetically silenced CDO1 resulted in restored expression and increased sensitivity to anthracyclines.
conclusionWe report that silencing of CDO1 is a critical epigenetic event that contributes to the survival of oxidative-stressed breast cancer cells through increased detoxification of ROS and thus leads to the resistance to ROS-generating chemotherapeutics including anthracyclines. Our study shows the importance of CDO1 inactivation in breast cancer and its clinical potential as a biomarker and therapeutic target to overcome resistance to anthracyclines.
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