ArticleMolecular pharmacology2010
Lyn kinase-dependent regulation of miR181 and myeloid cell leukemia-1 expression: implications for drug resistance in myelogenous leukemia.
Article in Molecular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
- Therapeutic Targets for Overcoming BCR::ABL1 Tyrosine Kinase Inhibitor Resistance in Chronic Myeloid Leukemia.Oncology research · 2026Review
- Profiling of miRNAs and their interfering targets in peripheral blood mononuclear cells from patients with chronic myeloid leukaemia.Frontiers in oncology · 2023Article
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- miR-181c regulates MCL1 and cell survival in GATA2 deficient cells.Journal of leukocyte biology · 2022Article
- Human and herpesvirus microRNAs in periodontal disease.Periodontology 2000 · 2021Review
- Vitamin D modulation and microRNAs in gastric cancer: prognostic and therapeutic role.Translational cancer research · 2021Review
- Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell.In vitro cellular & developmental biology. Animal · 2021Article
- miR-181d/RBP2/NF-κB p65 Feedback Regulation Promotes Chronic Myeloid Leukemia Blast Crisis.Frontiers in oncology · 2021Article
- Combinatorial Strategies to Target Molecular and Signaling Pathways to Disarm Cancer Stem Cells.Frontiers in oncology · 2021Review
- Metformin-induced suppression of Nemo-like kinase improves erythropoiesis in preclinical models of Diamond-Blackfan anemia through induction of miR-26a.Experimental hematology · 2020Article
- Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.Nature communications · 2020Article
- Lyn regulates creatine uptake in an imatinib-resistant CML cell line.Biochimica et biophysica acta. General subjects · 2020Article
- Comparison of microRNA Expression Profile in Chronic Myeloid Leukemia Patients Newly Diagnosed and Treated by Allogeneic Hematopoietic Stem Cell Transplantation.Frontiers in oncology · 2020Article
- Article
- Biological Aspects of mTOR in Leukemia.International journal of molecular sciences · 2018Review
- MicroRNAs and immunity in periodontal health and disease.International journal of oral science · 2018Review
- Post-Transcriptional Regulation of Anti-Apoptotic BCL2 Family Members.International journal of molecular sciences · 2018Review
- Combined targeting of STAT3 and STAT5: a novel approach to overcome drug resistance in chronic myeloid leukemia.Haematologica · 2017Article
- New insights into vitamin D anticancer properties: focus on miRNA modulation.Molecular genetics and genomics : MGG · 2017Review
- Induction of K562 Cell Apoptosis by As4S4 via Down-Regulating miR181.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Imatinib, a BCR-Abl inhibitor, is a successful front-line treatment for chronic myelogenous leukemia (CML). Despite the success of imatinib, multiple mechanisms of resistance remain a problem, including overexpression of Lyn kinase (Lyn) and Bcl-2 family antiapoptotic proteins. Profiling micro-RNA (miRNA) expression in a model of Lyn-mediated imatinib-resistant CML (MYL-R) identified approximately 30 miRNAs whose expression differed >2-fold compared with drug-sensitive MYL cells. In particular, the expression of the miR181 family (a-d) was significantly reduced (∼11- to 25-fold) in MYL-R cells. Incubation of MYL-R cells with a Lyn inhibitor (dasatinib) or nucleofection with Lyn-targeting short interfering RNA increased miR181b and miR181d expression. A similar Lyn-dependent regulation of miR181b and miR181d was observed in imatinib-resistant K562 CML cells. Sequence analysis of potential targets for miR181 regulation predicted myeloid cell leukemia-1 (Mcl-1), a Bcl-2 family member whose expression is increased in MYL-R cells and drug-resistant leukemias. Inhibition of Lyn or rescue of miR181b expression reduced Mcl-1 expression in the MYL-R cells. To further investigate the mechanism of Mcl-1 repression by miR181, a luciferase reporter construct incorporating the Mcl-1 3'-untranslated region was tested. Overexpression of miR181b reduced luciferase activity, whereas these effects were ablated by the mutation of the seed region of the miR181 target site. Finally, stimulation of Lyn expression by 1,25-dihydroxyvitamin D(3) treatment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and increased Mcl-1 expression. In summary, our results suggest that Lyn-dependent regulation of miR181 is a novel mechanism of regulating Mcl-1 expression and cell survival.
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Registered trials
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