ArticleLeukemia2022
Increased expression of RUNX3 inhibits normal human myeloid development.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Exploration of common genomic signatures of systemic juvenile rheumatoid arthritis and type 1 diabetes.Scientific reports · 2023Pooled it
- Expression of RUNX1::RUNX1T1 deregulates the proteome, induces C/EBPβ suppression, and blocks myeloid differentiation.Blood neoplasia · 2026Article
- Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- The Significance of RUNX3 Expression Levels in the Prognosis of Severe Acute Pancreatitis.International journal of general medicine · 2025Article
- Hematopoietic aging promotes cancer by fueling IL-1⍺-driven emergency myelopoiesis.Science (New York, N.Y.) · 2024Article
- Construction and validation of a SASP-related prognostic signature in patients with acute myeloid leukaemia.Journal of cellular and molecular medicine · 2024Article
- Article
- Integrated analysis and validation reveal CYTH4 as a potential prognostic biomarker in acute myeloid leukemia.Oncology letters · 2024Article
- Immune determinants of CAR-T cell expansion in solid tumor patients receiving GD2 CAR-T cell therapy.Cancer cell · 2024Article
- Article
- Transcriptomic Context ofBiomedicines · 2023Article
- Multimodal deep learning to predict prognosis in adult and pediatric brain tumors.Communications medicine · 2023Article
- Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
RUNX3 is a transcription factor dysregulated in acute myeloid leukemia (AML). However, its role in normal myeloid development and leukemia is poorly understood. Here we investigate RUNX3 expression in both settings and the impact of its dysregulation on myelopoiesis. We found that RUNX3 mRNA expression was stable during hematopoiesis but decreased with granulocytic differentiation. In AML, RUNX3 mRNA was overexpressed in many disease subtypes, but downregulated in AML with core binding factor abnormalities, such as RUNX1::ETO. Overexpression of RUNX3 in human hematopoietic stem and progenitor cells (HSPC) inhibited myeloid differentiation, particularly of the granulocytic lineage. Proliferation and myeloid colony formation were also inhibited. Conversely, RUNX3 knockdown did not impact the myeloid growth and development of human HSPC. Overexpression of RUNX3 in the context of RUNX1::ETO did not rescue the RUNX1::ETO-mediated block in differentiation. RNA-sequencing showed that RUNX3 overexpression downregulates key developmental genes, such as KIT and RUNX1, while upregulating lymphoid genes, such as KLRB1 and TBX21. Overall, these data show that increased RUNX3 expression observed in AML could contribute to the developmental arrest characteristic of this disease, possibly by driving a competing transcriptional program favoring a lymphoid fate.
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Registered trials
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