ArticleLeukemia2025
ADAR1 is required for acute myeloid leukemia cell survival by modulating post-transcriptional Wnt signaling through impairing miRNA biogenesis.
Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Targeting ADAR1 lactylation activates innate immune and overcomes chemoresistance in ovarian cancer.Cell death and differentiation · 2026Article
- The context-dependent role of the dsRNA response in linking A-to-I editing and ADAR to normal hematopoiesis and leukemia.Frontiers in cell and developmental biology · 2026Review
- The interplay between non-coding RNAs and Wnt signaling pathway in leukemia: A narrative review.BioImpacts : BI · 2026Review
- ZYS-1 is not an ADAR1 inhibitor.RNA (New York, N.Y.) · 2025Article
- HPCAL1 as a novel prognostic biomarker in acute myeloid leukemia and its correlation with immune infiltrates.Scientific reports · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- ADAR1-mediated RNA editing in breast cancer: molecular mechanisms and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025Review
- Deciphering the mechanistic roles of ADARs in cancer pathogenesis, tumor immune evasion, and drug resistance.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent extensive studies on the genomic and molecular profiles of acute myeloid leukemia (AML) have expanded the treatment options, including, a range of compounds represented by fms-like tyrosine kinase 3 and isocitrate dehydrogenase 1/2 inhibitors. However, despite this progress, further treatments for AML are still required. Adenosine deaminase acting on RNA 1 (ADAR1) has been shown to play an important oncogenic role in many cancers, but its involvement in AML progression remains underexplored. In this study, we demonstrated that ADAR1 was overexpressed in AML and served as a crucial oncogenic target. Loss of ADAR1 inhibited the Wnt signaling pathway, blocked AML cell proliferation, and induced apoptosis. Importantly, we demonstrate that ADAR1, as an RNA-binding protein, interacts with pri-miR-766 independently of its editing function, regulating the maturation of miR-766-3p and enhancing the expression of WNT5B. Genetic inhibition or use of the ADAR1 inhibitor ZYS-1 significantly suppressed AML cell growth both in vitro and in vivo. Overall, these results elucidated the tumorigenic mechanism of ADAR1 and validated it as a potential drug target in AML.
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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.