ArticleCell death & disease2025
Targeting METTL3 mitigates venetoclax resistance via proteasome-mediated modulation of MCL1 in acute myeloid leukemia.
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 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- Targeting epigenetic methylation: emerging diagnosis and therapeutic strategies in cancer.Experimental hematology & oncology · 2026Review
- The role of m6A RNA methyltransferase METTL3 in drug resistance mechanisms in acute myeloid leukemia.Blood research · 2026Review
- Mechanisms of astragalus polysaccharide enhancing STM2457 therapeutic efficacy in mMedical oncology (Northwood, London, England) · 2026Article
- Functional heterogeneity of TP53 mutants in venetoclax-resistant AML: mechanisms, clinical implications, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).Oncology reports · 2025Review
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Phytochemicals in overcoming venetoclax resistance in acute myeloid leukemia: mechanistic insights and therapeutic potential.Annals of hematology · 2025Review
- Epitranscriptomic control of cancer immunity and therapy resistance.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Venetoclax, a selective BCL2 inhibitor, is extensively utilized in clinical settings for the treatment of acute myeloid leukemia (AML). However, its efficacy is often compromised by the development of drug resistance. Hence, identification of potential venetoclax combination treatment strategies is imperative to overcome this acquired resistance. In this study, we discovered that inhibition of METTL3 can synergistically enhance the anti-leukemic efficacy of venetoclax, and is capable of overcoming venetoclax resistance in in vivo experiments and various venetoclax resistance models. Mechanistic study revealed that STM2457 augmented venetoclax activity by downregulating MCL1 and MYC, thereby increasing apoptosis in leukemia cells induced by venetoclax. Further investigation demonstrated that STM2457 promotes the ubiquitination and subsequent protein degradation of MCL1 primarily through pharmaceutically targeting METTL3. Moreover, through molecular docking-based virtual screening, we identified isoliquiritigenin as a potential novel small molecule natural product targeting METTL3, which exhibited potential effects as an anti-leukemic agent.
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Registered trials
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