ArticleCell reports. Medicine2024
Targeting DNMT3A-mediated oxidative phosphorylation to overcome ibrutinib resistance in mantle cell lymphoma.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanisms of resistance to BTK inhibitors in B cell malignancies and emerging targeted strategies.Molecular therapy. Oncology · 2026Review
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- BRG1-mediated suppression of ferroptosis underlies BTK inhibitor resistance.Nature communications · 2026Article
- Article
- Metabolic vulnerabilities and therapeutic opportunities in diffuse large B-cell lymphoma.Oncogenesis · 2026Review
- Prognostic Role of Global DNA Methylation in Renal Cancer Reveals Decitabine Treatment Benefit.Current medicinal chemistry · 2026Article
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- [IKZF3/Aiolos and tumors].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Inhibition of Retinoic Acid Receptor Gamma Improves Bovine Embryo Development.Veterinary sciences · 2025Article
- High oxidative phosphorylation represented by UQCRFS1 marks CD8 + tumor-infiltrating lymphocytes exhaustion in diffuse large B-cell lymphoma.Biology direct · 2025Article
- Molecular pathology of lymphoma and its treatment strategies: from mechanistic elucidation to precision medicine.Frontiers in immunology · 2025Review
- Macrophage Membrane-Coated Liposomes Delivering Vonoprazan Disrupt Mitochondrial Oxidative Phosphorylation in Diffuse Large B-Cell Lymphoma.International journal of nanomedicine · 2025Article
- Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
The use of Bruton tyrosine kinase (BTK) inhibitors such as ibrutinib achieves a remarkable clinical response in mantle cell lymphoma (MCL). Acquired drug resistance, however, is significant and affects long-term survival of MCL patients. Here, we demonstrate that DNA methyltransferase 3A (DNMT3A) is involved in ibrutinib resistance. We find that DNMT3A expression is upregulated upon ibrutinib treatment in ibrutinib-resistant MCL cells. Genetic and pharmacological analyses reveal that DNMT3A mediates ibrutinib resistance independent of its DNA-methylation function. Mechanistically, DNMT3A induces the expression of MYC target genes through interaction with the transcription factors MEF2B and MYC, thus mediating metabolic reprogramming to oxidative phosphorylation (OXPHOS). Targeting DNMT3A with low-dose decitabine inhibits the growth of ibrutinib-resistant lymphoma cells both in vitro and in a patient-derived xenograft mouse model. These findings suggest that targeting DNMT3A-mediated metabolic reprogramming to OXPHOS with decitabine provides a potential therapeutic strategy to overcome ibrutinib resistance in relapsed/refractory MCL.
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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.