ArticleOncology letters2025
Ferroptosis as a therapeutic vulnerability in MDM2 inhibition in dedifferentiated liposarcoma.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
1 citing paper in PubMed.
- Dedifferentiated liposarcoma presenting with ascites as the initial clinical manifestation: a case report and literature review.Frontiers in medicine · 2026Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a form of necrotic cell death characterized by phospholipid oxidation. The cystine-glutamate antiporter (xCT), composed of solute carrier family 7 member 11 (SLC7A11) and SLC3A2, imports cystine for glutathione synthesis. Glutathione peroxidase 4 (GPX4) requires glutathione to counteract lipid peroxidation and prevent ferroptosis. Erastin, an xCT inhibitor, and Ras-selective lethal small molecule 3 (RSL3), a GPX4 inhibitor, suppress GPX4 function and induce ferroptosis. Tumor protein p53 (TP53) has a paradoxical role in ferroptosis regulation. Mouse double minute 2 homolog (MDM2), a negative regulator of TP53, is a key oncogene in well-differentiated liposarcoma (WDLPS) and dedifferentiated liposarcoma (DDLPS). Therefore, the present study explored the role of ferroptosis in DDLPS treatment response and resistance. Publicly available expression profiles of WDLPS, DDLPS and adipose tissue were analyzed, and the differential expression of ferroptosis-related genes regulated by the MDM2-TP53 pathway was identified in WDLPS and DDLPS.
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