ArticleCell death & disease2025
Mechanisms of chemotherapy failure in refractory/relapsed acute myeloid leukemia: the role of cytarabine resistance and mitochondrial metabolism.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Transcriptomic profiling and structural characterization reveal UQCRC1 and COX4I1 as key mitochondrial regulators associated with oxidative stress in multiple sclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.Journal of translational medicine · 2026Article
- Mesothelin promotes acute myeloid leukemia progression through LYN-dependent signaling.The Journal of biological chemistry · 2026Article
- Enhancing the Nucleoside Analog Response with Translational Therapeutic Approaches to Overcome Resistance.Cells · 2026Review
- PDCD4: A critical regulator in leukemic signaling networks and its therapeutic potential.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Acute myeloid leukemia (AML) is an aggressive hematological malignancy. Patients with wild-type FLT3 relapsed or refractory (R/R) AML face significant therapeutic challenges due to the persistent lack of effective treatments. A comprehensive understanding of the mechanisms underlying chemotherapy resistance is needed to the development of effective treatment strategies. Therefore, we investigated the molecular mechanisms underlying cytarabine (Ara-C) resistance and daunorubicin (DNR) tolerance in Ara-C-resistant RHI-1 cells derived from the wild-type FLT3 AML cell line SHI-1. Quantitative analysis of intracellular drug concentrations, proteomics, and phosphoproteomics showed that DNR resistance in Ara-C-resistant RHI-1 cells is driven by metabolic remodeling toward mitochondrial metabolism, upregulation of DNA repair pathways, and enhanced reactive oxygen species (ROS) detoxification rather than reduced drug uptake. Moreover, targeting these compensatory mechanisms, particularly the OXPHOS complex I proteins, significantly improved the efficacy of both Ara-C and DNR. Conclusively, these findings highlight mitochondrial metabolism and DNA repair as critical factors in chemotherapy resistance and offer valuable insights into potential therapeutic targets for enhancing treatment outcomes in patients with wild-type FLT3 R/R AML.
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