ArticleExperimental biology and medicine (Maywood, N.J.)2016
Original Research: Stable expression of miR-34a mediates fetal hemoglobin induction in K562 cells.
Article in Experimental biology and medicine (Maywood, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- The role of hydroxyurea in modulating miRNA expression in sickle cell disease: molecular mechanisms and therapeutic implications.Annals of hematology · 2026Review
- Clinical value of miR-329-3p in thalassemia and its regulation of TNRC6B expression.Annals of hematology · 2026Article
- Review
- Cholesterol-conjugated miR-29b induces fetal haemoglobin expression via γ-globin promoter demethylation in the Townes mouse model for sickle cell anaemia.British journal of haematology · 2025Article
- Evaluation of Genes and Molecular Pathways Involved in Pathogenesis of Sickle Cell Anemia: A Bioinformatics Analysis and Future Perspective.Iranian journal of public health · 2024Article
- Pharmacogenomics of Drugs Used in β-Thalassemia and Sickle-Cell Disease: From Basic Research to Clinical Applications.International journal of molecular sciences · 2024Review
- Review
- Targeting Genetic Modifiers of HBG Gene Expression in Sickle Cell Disease: The miRNA Option.Molecular diagnosis & therapy · 2022Review
- MicroRNAs and JAK/STAT3 signaling: A new promising therapeutic axis in blood cancers.Genes & diseases · 2022Review
- Bioinformatic Tools for the Identification of MicroRNAs Regulating the Transcription Factors in Patients with β-Thalassemia.Bioinformatics and biology insights · 2022Review
- MicroRNA29B induces fetal hemoglobinFrontiers in medicine · 2022Article
- Article
- Exploring epigenetic and microRNA approaches for γ-globin gene regulation.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- The Role of miRNAs as Therapeutic Tools in Sickle Cell Disease.Medicina (Kaunas, Lithuania) · 2021Review
- Distinct miRNA Signatures and Networks Discern Fetal from Adult Erythroid Differentiation and Primary from Immortalized Erythroid Cells.International journal of molecular sciences · 2021Article
- miR-30a regulates γ-globin expression in erythoid precursors of intermedia thalassemia through targeting BCL11A.Molecular biology reports · 2020Article
- MIR29B mediates epigenetic mechanisms of HBG gene activation.British journal of haematology · 2019Article
- MIR-144-mediated NRF2 gene silencing inhibits fetal hemoglobin expression in sickle cell disease.Experimental hematology · 2019Article
- Mechanisms of NRF2 activation to mediate fetal hemoglobin induction and protection against oxidative stress in sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Fetal hemoglobin induction in sickle erythroid progenitors using a synthetic zinc finger DNA-binding domain.Haematologica · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sickle cell anemia is a common genetic disorder caused by a point mutation in the sixth codon of the β-globin gene affecting people of African descent worldwide. A wide variety of clinical phenotypes ranging from mild to severe symptoms and complications occur due to hemoglobin S polymerization, red blood cell sickling, and vaso-occlusion. Research efforts are ongoing to develop strategies of fetal hemoglobin (HbF; α2γ2) induction to inhibit sickle hemoglobin polymerization and improve clinical outcomes. Insights have been gained from investigating mutations in the β-globin locus or transcription factors involved in the mechanisms of hemoglobin switching. Recent efforts to expand molecular targets that modulate γ-globin expression involve microRNAs that work through posttranscriptional gene regulation. Therefore, the goal of our study was to identify novel microRNA genes involved in fetal hemoglobin expression. Using in silico analysis, we identified a miR-34a binding site in the γ-globin mRNA which was tested for functional relevance. Stable expression of the shMIMIC miR-34a lentivirus vector increased fetal hemoglobin levels in single cell K562 clones consistent with silencing of a γ-globin gene repressor. Furthermore, miR-34a promoted cell differentiation supported by increased expression of KLF1, glycophorin A, and the erythropoietin receptor. Western blot analysis of known negative regulators of γ-globin including YY1, histone deacetylase 1, and STAT3, which are regulated by miR-34a showed no change in YY1 and histone deacetylase 1 levels; however, total- and phosphorylated-STAT3 levels were decreased in single cell miR-34a K562 clones. These data support a mechanism of fetal hemoglobin activation by miR-34a involving STAT3 gene silencing.
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Registered trials
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