ArticleBlood2014
miRNA-mRNA integrative analysis in primary myelofibrosis CD34+ cells: role of miR-155/JARID2 axis in abnormal megakaryopoiesis.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 123 citations in OpenAlex.
- Review
- A stem and progenitor cell-derived gene expression signature is prognostic for survival in myelofibrosis.Blood · 2026Article
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress.Molecular cancer research : MCR · 2024Article
- A let-7 microRNA-RALB axis links the immune properties of iPSC-derived megakaryocytes with platelet producibility.Nature communications · 2024Article
- MiR-155 promotes compensatory lung growth by inhibiting JARID2 activation of CD34+ endothelial progenitor cells.PloS one · 2024Article
- Complementary and countervailing actions of Jak2 and Ikk2 in hematopoiesis in mice.Experimental hematology · 2023Article
- Biological drivers of clinical phenotype in myelofibrosis.Leukemia · 2023Review
- DUSP6 mediates resistance to JAK2 inhibition and drives leukemic progression.Nature cancer · 2023Article
- Novel Molecular Insights into Leukemic Evolution of Myeloproliferative Neoplasms: A Single Cell Perspective.International journal of molecular sciences · 2022Review
- Exploring links between 2-oxoglutarate-dependent oxygenases and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Review
- Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm.Nature communications · 2022Article
- Inhibition of interleukin-1β reduces myelofibrosis and osteosclerosis in mice with JAK2-V617F driven myeloproliferative neoplasm.Nature communications · 2022Article
- MicroRNAs and JAK/STAT3 signaling: A new promising therapeutic axis in blood cancers.Genes & diseases · 2022Review
- Expression profiles analysis identifies specific interferon-stimulated signatures as potential diagnostic and predictive indicators ofFrontiers in genetics · 2022Article
- Article
- A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms.Cancer discovery · 2021Article
- New Markers of Disease Progression in Myelofibrosis.Cancers · 2021Review
- Gene expression profile correlates with molecular and clinical features in patients with myelofibrosis.Blood advances · 2021Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
26 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by megakaryocyte (MK) hyperplasia, bone marrow fibrosis, and abnormal stem cell trafficking. PMF may be associated with somatic mutations in JAK2, MPL, or CALR. Previous studies have shown that abnormal MKs play a central role in the pathophysiology of PMF. In this work, we studied both gene and microRNA (miRNA) expression profiles in CD34(+) cells from PMF patients. We identified several biomarkers and putative molecular targets such as FGR, LCN2, and OLFM4. By means of miRNA-gene expression integrative analysis, we found different regulatory networks involved in the dysregulation of transcriptional control and chromatin remodeling. In particular, we identified a network gathering several miRNAs with oncogenic potential (eg, miR-155-5p) and targeted genes whose abnormal function has been previously associated with myeloid neoplasms, including JARID2, NR4A3, CDC42, and HMGB3. Because the validation of miRNA-target interactions unveiled JARID2/miR-155-5p as the strongest relationship in the network, we studied the function of this axis in normal and PMF CD34(+) cells. We showed that JARID2 downregulation mediated by miR-155-5p overexpression leads to increased in vitro formation of CD41(+) MK precursors. These findings suggest that overexpression of miR-155-5p and the resulting downregulation of JARID2 may contribute to MK hyperplasia in PMF.
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