ArticleScientific reports2017
Autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting Runx1 Slows Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- PROTACs coupled with oligonucleotides to tackle the undruggable.Bioanalysis · 2025Review
- Tyr-Tyr-Glu Tripeptide for Regeneration of Articular Cartilage through Chondrogenic Differentiation of Mesenchymal Stem Cells.Biomaterials research · 2025Article
- Modeling and therapeutic targeting of t(8;21) AML with/without TP53 deficiency.International journal of hematology · 2024Article
- Mesenchymal stem cells and dental implant osseointegration during aging: from mechanisms to therapy.Stem cell research & therapy · 2023Review
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.The veterinary quarterly · 2023Article
- RUNX1-Regulated Signaling Pathways in Ovarian Cancer.Biomedicines · 2023Review
- Review
- Review
- RUNX1-Survivin Axis Is a Novel Therapeutic Target for Malignant Rhabdoid Tumors.Molecules and cells · 2022Article
- A RUNX-targeted gene switch-off approach modulates the BIRC5/PIF1-p21 pathway and reduces glioblastoma growth in mice.Communications biology · 2022Article
- Molecular Classification and Overcoming Therapy Resistance for Acute Myeloid Leukemia with Adverse Genetic Factors.International journal of molecular sciences · 2022Review
- RUNX1 transactivates BCR-ABL1 expression in Philadelphia chromosome positive acute lymphoblastic leukemia.Cancer science · 2022Article
- Cancer-Associated Exosomal CBFB Facilitates the Aggressive Phenotype, Evasion of Oxidative Stress, and Preferential Predisposition to Bone Prometastatic Factor of Breast Cancer Progression.Disease markers · 2022Article
- Runt-related transcription factor 1 (Runx1) aggravates pathological cardiac hypertrophy by promoting p53 expression.Journal of cellular and molecular medicine · 2021Article
- Integrated analysis of microRNA and transcription factors in the bone marrow of patients with acute monocytic leukemia.Oncology letters · 2021Article
- Identification of a prognostic signature based on copy number variations (CNVs) and CNV-modulated gene expression in acute myeloid leukemia.American journal of translational research · 2021Article
- Functional Dependency Analysis Identifies Potential Druggable Targets in Acute Myeloid Leukemia.Cancers · 2020Article
- Screening potential microRNAs associated with pancreatic cancer: Data mining based on RNA sequencing and microarrays.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Although runt-related transcription factor 1 (RUNX1) and its associating core binding factor-β (CBFB) play pivotal roles in leukemogenesis, and inhibition of RUNX1 has now been widely recognized as a novel strategy for anti-leukemic therapies, it has been elusive how leukemic cells could acquire the serious resistance against RUNX1-inhibition therapies and also whether CBFB could participate in this process. Here, we show evidence that p53 (TP53) and CBFB are sequentially up-regulated in response to RUNX1 depletion, and their mutual interaction causes the physiological resistance against chemotherapy for acute myeloid leukemia (AML) cells. Mechanistically, p53 induced by RUNX1 gene silencing directly binds to CBFB promoter and stimulates its transcription as well as its translation, which in turn acts as a platform for the stabilization of RUNX1, thereby creating a compensative RUNX1-p53-CBFB feedback loop. Indeed, AML cells derived from relapsed cases exhibited higher CBFB expression levels compared to those from primary AML cells at diagnosis, and these CBFB expressions were positively correlated to those of p53. Our present results underscore the importance of RUNX1-p53-CBFB regulatory loop in the development and/or maintenance of AML cells, which could be targeted at any sides of this triangle in strategizing anti-leukemia therapies.
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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.