ArticleEuropean journal of medical research2025
GDF-15 upregulates the SLC7A11/GPX4 signaling axis and promotes mitoxantrone resistance in AML cells.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.Cell cycle (Georgetown, Tex.) · 2026Article
- Apoptosis-related gene model predicts the prognosis in patients with acute myeloid leukemia.Blood science (Baltimore, Md.) · 2026Article
- Statistical Inference of Phenotype-Specific Molecular Mechanisms from Cell Line-Specific Gene Regulatory Networks with Application to Quizartinib Sensitivity.International journal of molecular sciences · 2026Article
- Growth Differentiation Factor 15 (GDF-15) as a modulator of hepatic steatosis and fibrosis: insights from a 6-year retrospective cohort study.Frontiers in medicine · 2026Article
- Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).Oncology reports · 2025Review
- Non-coding RNAs-regulated SLC7A11 modulates ferroptosis: a new strategy for cancer therapy.Functional & integrative genomics · 2025Review
- Ferroptosis: a novel pharmacological mechanism against multiple myeloma.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
Chemotherapy resistance poses a significant challenge in the initial treatment of acute myeloid leukemia (AML). Growth differentiation factor 15 (GDF-15) has been shown to play a critical role in cancer progression; however, the potential mechanisms by which GDF-15 contributes to AML progression and chemotherapy resistance remain unclear. We found that M2 macrophages secrete high levels of GDF-15, promoting resistance of AML cells to mitoxantrone (MTX). Furthermore, we demonstrated that MTX induces downregulation of the SLC7A11/GPX4 signaling axis in AML cells, mediating ferroptosis. GDF-15 enhances the expression of the SLC7A11/GPX4 axis, thereby inhibiting ferroptosis in AML cells and contributing to drug resistance. In addition, GDF-15 mitigates the decline in mitochondrial membrane potential and mitochondrial quality induced by MTX. In vivo experiments indicate that blocking GDF-15 effectively enhances the sensitivity of AML cells to mitoxantrone by reducing the expression of the SLC7A11/GPX4 axis.
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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 Socratic graph.