ArticleClinical and experimental medicine2025
CDC26 facilitates ferroptosis through SLC7A11 degradation and cell cycle arrest.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pharmacological targeting of ferroptosis in cancer: mechanisms, tumor immunity, and translational challenges.Pharmacological reports : PR · 2026Review
- Repurposing dronedarone induces ferroptosis through GPX4 inactivation and degradation in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- An integrated analysis of SLC7A11 as a pan-cancer immunotherapeutic biomarker with experimental validation of its regulation by miR-148b-3p in breast cancer.Frontiers in immunology · 2026Article
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9 authors.
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Abstract
The ubiquitin proteasome system serves as one of the key protein degradation pathways for cellular homeostasis, and its E3 ubiquitin ligase regulates cell survival and death by specifically recognizing the degradation of target proteins. Ferroptosis, a regulated cell death driven by membrane lipid peroxidation, is modulated by the ubiquitin-proteasome system through E3 ubiquitin ligases targeting specific proteins. Based on the screening of 571 UPS-related genes in previous studies, we further selected a subset of 286 E3 ligases for analysis. Subsequently, cell division cycle 26 (CDC26) was identified as an inducer of ferroptosis in in human pancreatic ductal adenocarcinoma (PDAC) cells. CDC26 expression is downregulated during ferroptosis in PDAC. Functionally, CDC26 overexpression enhances ferroptosis by increasing reactive oxygen species (ROS) and lipid peroxidation, while suppressing cell proliferation and invasion. Mechanistically, CDC26 promotes the ubiquitin-mediated degradation of solute carrier family 7 member 11 (SLC7A11), a key ferroptosis inhibitor, and indirectly inhibits the cell cycle, further sensitizing cells to ferroptosis. These findings establish CDC26 as a ferroptosis mediator, highlighting its role in the ubiquitin-proteasome-ferroptosis network and its potential as a therapeutic target for pancreatic cancer.
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