ArticleBlood2019
circMYBL2, a circRNA from MYBL2, regulates FLT3 translation by recruiting PTBP1 to promote FLT3-ITD AML progression.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.
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Who cites it
150 citing papers in PubMed, 279 citations in OpenAlex.
- Article
- PTBP1 controls oncogenic transcript processing and maintenance of acute myeloid leukemia.Leukemia · 2026Article
- CircHECTD1 Promotes Cholangiocarcinoma Progression Through Interaction With SFPQ to Induce Autophagy.Cancer science · 2026Article
- Genome-wide investigation of differentially expressed alternative splicing and RNA-binding protein genes association with AML drug resistance.Discover oncology · 2026Article
- Assessing the contributions of noncoding RNAs in acute myeloid leukemia.Blood neoplasia · 2026Review
- EIF4A3-induced circUBAC2 promotes lung cancer progression via regulation of the Hippo signaling pathway.Cellular & molecular biology letters · 2026Article
- Landscape of circular RNAs in acute myeloid leukemia and their clinical significance.NPJ precision oncology · 2026Article
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- A novel microprotein MUCP1 promotes colorectal cancer metabolic reprogramming by regulating mitochondrial succinate transport.Neoplasia (New York, N.Y.) · 2026Article
- RBM15B recognizes H3K79me2 to guide selective mThe EMBO journal · 2026Article
- The therapeutic potential and mechanisms of targeting the PTBP1/Nogo-A/NgR axis in PTSD induced by single prolonged stress in mice.Experimental & molecular medicine · 2026Article
- Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis.Journal of advanced research · 2026Article
- Chromatin-associated circRNA ciCRLF3(2) regulates cell differentiation blockage via activating non-homologous end joining-based DNA repair.Cell death and differentiation · 2026Article
- Machine learning prediction for AML based on 3D genome selected circRNA.NPJ systems biology and applications · 2026Article
- The splicing factor PTBP1 interacts with RUNX1 and is required for leukemia cell survival.Leukemia · 2026Article
- Circular RNA circMYBL2 regulates the progression of ovarian cancer through miR-195-5P/BIRC5 axis.Journal of ovarian research · 2025Article
- Accurate Reconstruction of Circular RNAs from Complex Rolling Circular Long Reads with CircPlex.bioRxiv : the preprint server for biology · 2025Article
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- CircPPP1CB subtype, hsa_circ_0007439, promotes nasopharyngeal carcinoma progression by upregulating KRT1.Discover oncology · 2025Article
- Targeting p16Leukemia · 2025Article
90 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Internal tandem duplication (ITD) mutations within FMS-like tyrosine kinase-3 (FLT3) occur in up to 30% of acute myeloid leukemia (AML) patients and confer a very poor prognosis. The oncogenic form of FLT3 is an important therapeutic target, and inhibitors specifically targeting FLT3 kinase can induce complete remission; however, relapse after remission has been observed due to acquired resistance with secondary mutations in FLT3, highlighting the need for new strategies to target FLT3-ITD mutations. Recent studies have reported that the aberrant formations of circular RNAs (circRNAs) are biological tumorigenesis-relevant mechanisms and potential therapeutic targets. Herein, we discovered a circRNA, circMYBL2, derived from the cell-cycle checkpoint gene MYBL2. circMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. Mechanistically, circMYBL2 enhanced the translational efficiency of FLT3 kinase by increasing the binding of polypyrimidine tract-binding protein 1 (PTBP1) to FLT3 messenger RNA. Moreover, circMYBL2 knockdown impaired the cytoactivity of inhibitor-resistant FLT3-ITD+ cells, with a significant decrease in FLT3 kinase expression, followed by the inactivation of its downstream pathways. In summary, we are the first to reveal a circRNA that specifically influences FLT3-ITD AML and regulates FLT3 kinase levels through translational regulation, suggesting that circMYBL2 may be a potential therapeutic target for FLT3-ITD AML.
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