ArticleProceedings of the National Academy of Sciences of the United States of America2010
Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Investigation Role of Toll-like Receptor-9 Gene and miR-155 Expression Levels in Acute Myeloid Leukemia via Quantitative Real-Time PCR.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.Blood cancer journal · 2021Review
- Review
- Review
- Expression and prognostic significance of microRNAs in Korean patients with myelodysplastic syndrome.The Korean journal of internal medicine · 2019Article
- β-Amyloid triggers aberrant over-scaling of homeostatic synaptic plasticity.Acta neuropathologica communications · 2016Article
- Epigenetic regulation of miRNA-124 and multiple downstream targets is associated with treatment response in myeloid malignancies.Oncology letters · 2016Article
- MicroRNAs as regulatory elements in immune system logic.Nature reviews. Immunology · 2016Review
- MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity.Nature communications · 2015Article
- Digging deep into "dirty" drugs - modulation of the methylation machinery.Drug metabolism reviews · 2015Review
- Methylation and microRNA-mediated epigenetic regulation of SOCS3.Molecular biology reports · 2015Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
- MicroRNA Clusters in the Adult Mouse Heart: Age-Associated Changes.BioMed research international · 2015Article
- EVI1 oncogene promotes KRAS pathway through suppression of microRNA-96 in pancreatic carcinogenesis.Oncogene · 2014Article
- MicroRNA-155 as an inducer of apoptosis and cell differentiation in Acute Myeloid Leukaemia.Molecular cancer · 2014Article
- EVI1 splice variants modulate functional responses in ovarian cancer cells.Molecular oncology · 2013Article
- Epigenetic alterations and microRNAs: new players in the pathogenesis of myelodysplastic syndromes.Epigenetics · 2013Review
- Critical role of miR-9 in myelopoiesis and EVI1-induced leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?Haematologica · 2013Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
By expressing EVI1 in murine bone marrow (BM), we previously described a myelodysplastic syndrome (MDS) model characterized by pancytopenia, dysmegakaryopoiesis, dyserythropoiesis, and BM failure. The mice invariably died 11-14 months after BM transplantation (BMT). Here, we show that a double point mutant EVI1-(1+6Mut), unable to bind Gata1, abrogates the onset of MDS in the mouse and re-establishes normal megakaryopoiesis, erythropoiesis, BM function, and peripheral blood profiles. These normal features were maintained in the reconstituted mice until the study was ended at 21 months after BMT. We also report that EVI1 deregulates several genes that control cell division and cell self-renewal. In striking contrast, these genes are normalized in the presence of the EVI1 mutant. Moreover, EVI1, but not the EVI1 mutant, seemingly deregulates these cellular processes by altering miRNA expression. In particular, the silencing of miRNA-124 by DNA methylation is associated with EVI1 expression, but not that of the EVI1 mutant, and appears to play a key role in the up-regulation of cell division in murine BM cells and in the hematopoietic cell line 32Dcl3. The results presented here demonstrate that EVI1 induces MDS in the mouse through two major pathways, both of which require the interaction of EVI1 with other factors: one, results from EVI1-Gata1 interaction, which deregulates erythropoiesis and leads to fatal anemia, whereas the other occurs by interaction of EVI1 with unidentified factors causing perturbation of the cell cycle and self-renewal, as a consequence of silencing miRNA-124 by EVI1 and, ultimately, ensues in BM failure.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.