ArticleCell death & disease2017
Knockdown of miR-128a induces Lin28a expression and reverts myeloid differentiation blockage in acute myeloid leukemia.
Article in Cell death & disease, 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, 43 citations in OpenAlex.
- Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1.Theranostics · 2026Article
- The multiplex crosstalk between non-coding RNAs, programmed cell death and related mechanisms: a dynamic duo in hematological malignancies.Cancer cell international · 2025Review
- The up-regulation of TGF-β1 by miRNA-132-3p/WT1 is involved in inducing leukemia cells to differentiate into macrophages.PloS one · 2025Article
- The role of Lin28A and Lin28B in cancer beyond Let-7.FEBS letters · 2024Review
- Recent advancements in biomarkers, therapeutics, and associated challenges in acute myeloid leukemia.Annals of hematology · 2024Review
- A novel therapeutic strategy: the significance of exosomal miRNAs in acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2024Review
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Haematopoietic stem and progenitor cell heterogeneity is inherited from the embryonic endothelium.Nature cell biology · 2023Article
- Article
- MicroRNAs, Tristetraprolin Family Members and HuR: A Complex Interplay Controlling Cancer-Related Processes.Cancers · 2022Review
- Emerging Roles of RNA-Binding Proteins in Neurodevelopment.Journal of developmental biology · 2022Review
- Clinical Value of Serum miRNA in Patients with Acute Promyelocytic Leukemia.Journal of oncology · 2022Article
- Acute Myeloid Leukemia Cells Functionally Compromise Hematopoietic Stem/Progenitor Cells Inhibiting Normal Hematopoiesis Through the Release of Extracellular Vesicles.Frontiers in oncology · 2022Article
- Overexpression of Lin28A in neural progenitor cells in vivo does not lead to brain tumor formation but results in reduced spine density.Acta neuropathologica communications · 2021Article
- LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit.Cell death & disease · 2021Article
- Clinical relevance of extracellular vesicles in hematological neoplasms: from liquid biopsy to cell biopsy.Leukemia · 2021Review
- Lin28A/CENPE Promoting the Proliferation and Chemoresistance of Acute Myeloid Leukemia.Frontiers in oncology · 2021Article
- Review
- Article
- Ailanthone: A novel potential drug for treating human cancer.Oncology letters · 2020Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lin28A is a highly conserved RNA-binding protein that concurs to control the balance between stemness and differentiation in several tissue lineages. Here, we report the role of miR-128a/Lin28A axis in blocking cell differentiation in acute myeloid leukemia (AML), a genetically heterogeneous disease characterized by abnormally controlled proliferation of myeloid progenitor cells accompanied by partial or total inability to undergo terminal differentiation. First, we found Lin28A underexpressed in blast cells from AML patients and AML cell lines as compared with CD34+ normal precursors. In vitro transfection of Lin28A in NPM1-mutated OCI-AML3 cell line significantly triggered cell-cycle arrest and myeloid differentiation, with increased expression of macrophage associate genes (EGR2, ZFP36 and ANXA1). Furthermore, miR-128a, a negative regulator of Lin28A, was found overexpressed in AML cells compared with normal precursors, especially in acute promyelocytic leukemia (APL) and in 'AML with maturation' (according to 2016 WHO classification of myeloid neoplasms and acute leukemia). Its forced overexpression by lentiviral infection in OCI-AML3 downregulated Lin28A with ensuing repression of macrophage-oriented differentiation. Finally, knockdown of miR-128a in OCI-AML3 and in APL/AML leukemic cells (by transfection and lentiviral infection, respectively) induced myeloid cell differentiation and increased expression of Lin28A, EGR2, ZFP36 and ANXA1, reverting myeloid differentiation blockage. In conclusion, our findings revealed a new mechanism for AML differentiation blockage, suggesting new strategies for AML therapy based upon miR-128a inhibition.
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