ArticleMolecular cancer2025
Metabolic reprogramming promotes apoptosis resistance in acute lymphoblastic leukemia through CASP3 lactylation.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- β3-adrenergic blockade targets fatty acid oxidation to induce ferroptotic vulnerability in pediatric T-ALL.Biology direct · 2026Article
- Lysine lactylation-mediated post-translational modification: Molecular mechanisms and therapeutic target exploration in tumour drug resistance.Clinical and translational medicine · 2026Review
- Lactylation of PTBP1 drives a pro-apoptotic positive feedback loop in microglia following oxygen-glucose deprivation/reoxygenation-induced injury.Cell death & disease · 2026Article
- Protein lactylation: a metabolic signal driving cancer therapy resistance.Cell death discovery · 2026Review
- Dynamic regulation of TBK1 lactylation shapes antiviral immune responses.Cellular & molecular immunology · 2026Article
- Lactylation in cancer: molecular mechanisms and advances in clinical study.Molecular cancer · 2026Review
- Lactic Acid in Tumour Biology.Metabolites · 2026Review
- Integrating single-cell analysis and machine learning algorithms to explore lactylation-related molecular mechanisms and therapeutic responses in clear cell renal cell carcinoma and identifying CDT1 as a potential biomarker.Frontiers in endocrinology · 2026Article
- Targeting Lactylation Offers Therapy to Reverse Cell Death Resistance.Drug design, development and therapy · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Acute lymphoblastic leukemia (ALL) is characterized by metabolic adaptations that support rapid cell proliferation and resistance to apoptosis. Our study identifies elevated sphingomyelin (SM) as a key metabolic alteration in ALL, contributing to apoptosis resistance via CASP3 (caspase 3) lactylation. Using comprehensive lipidomic analyses of plasma samples from pediatric ALL patients, we observed significantly increased SM concentrations in patients with manifest ALL compared to patients after remission. Mechanistic investigations revealed that elevated SM enhances SLC2A1-dependent glucose uptake and glycolysis, leading to increased lactate production and subsequent CASP3 lactylation on lysine residue 14, which inhibits CASP3 activation and apoptosis. Reduction of intracellular SM levels through SGMS1 knockout or SMPD3 overexpression reduced glycolytic flux and lactate levels, restored CASP3 activity and induced apoptosis in ALL cells. In vivo, SM depletion significantly suppressed ALL progression and prolonged survival in mouse models, highlighting the potential of targeting SM metabolism as a therapeutic strategy. In conclusion, our findings uncover a metabolic pathway linking lipid and glucose metabolism to apoptosis resistance in ALL.
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Registered trials
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 OpenQuestion graph.