ArticleNeoplasia (New York, N.Y.)2010
Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.
Article in Neoplasia (New York, N.Y.), 2010. 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, 37 citations in OpenAlex.
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- MiRNA therapeutics based on logic circuits of biological pathways.BMC bioinformatics · 2019Article
- Aberrant Expression of the miR-181b/miR-222 after Hematopoietic Stem Cell Transplantation in Patients with Acute Myeloid Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2019Article
- Gene expression analyses determine two different subpopulations in KIT-negative GIST-like (KNGL) patients.Oncotarget · 2018Article
- PAX3-FOXO1 drives miR-486-5p and represses miR-221 contributing to pathogenesis of alveolar rhabdomyosarcoma.Oncogene · 2018Article
- MicroRNAs as New Biomarkers for Diagnosis and Prognosis, and as Potential Therapeutic Targets in Acute Myeloid Leukemia.International journal of molecular sciences · 2018Review
- Putative genomic characteristics of BRAF V600K versus V600E cutaneous melanoma.Melanoma research · 2017Article
- Article
- MiR144/451 Expression Is Repressed by RUNX1 During Megakaryopoiesis and Disturbed by RUNX1/ETO.PLoS genetics · 2016Article
- MicroRNAs in Myeloid Hematological Malignancies.Current genomics · 2015Article
- miR-17 deregulates a core RUNX1-miRNA mechanism of CBF acute myeloid leukemia.Molecular cancer · 2015Article
- Silencing AML1-ETO gene expression leads to simultaneous activation of both pro-apoptotic and proliferation signaling.Leukemia · 2014Article
- Increased expression of miR-24 is associated with acute myeloid leukemia with t(8;21).International journal of clinical and experimental pathology · 2014Article
- Long and short non-coding RNAs as regulators of hematopoietic differentiation.International journal of molecular sciences · 2013Review
- RUNX1: A microRNA hub in normal and malignant hematopoiesis.International journal of molecular sciences · 2013Review
- Regeneration-associated WNT signaling is activated in long-term reconstituting AC133bright acute myeloid leukemia cells.Neoplasia (New York, N.Y.) · 2012Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.Frontiers of medicine · 2012Review
- Prognostic markers in AML: focus on CBFL.Leukemia supplements · 2012Article
- The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity.Journal of mammary gland biology and neoplasia · 2012Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Core-binding factor leukemia (CBFL) is a subgroup of acute myeloid leukemia (AML) characterized by genetic mutations involving the subunits of the core-binding factor (CBF). The leukemogenesis model for CBFL posits that one, or more, gene mutations inducing increased cell proliferation and/or inhibition of apoptosis cooperate with CBF mutations for leukemia development. One of the most common mutations associated with CBF mutations involves the KIT receptor. A high expression of KIT is a hallmark of a high proportion of CBFL. Previous studies indicate that microRNA (MIR) 222/221 targets the 3' untranslated region of the KIT messenger RNA and our observation that AML1 can bind the MIR-222/221 promoter, we hypothesized that MIR-222/221 represents the link between CBF and KIT. Here, we show that MIR-222/221 expression is upregulated after myeloid differentiation of normal bone marrow AC133(+) stem progenitor cells. CBFL blasts with either t(8;21) or inv(16) CBF rearrangements with high expression levels of KIT (CD117) display a significantly lower level of MIR-222/221 expression than non-CBFL blasts. Consistently, we found that the t(8;21) AML1-MTG8 fusion protein binds the MIR-222/221 promoter and induces transcriptional repression of a MIR-222/221-LUC reporter. Because of the highly conserved sequence homology, we demonstrated concomitant MIR-222/221 down-regulation and KIT up-regulation in the 32D/WT1 mouse cell model carrying the AML1-MTG16 fusion protein. This study provides the first hint that CBFL-associated fusion proteins may lead to up-regulation of the KIT receptor by down-regulating MIR-222/221, thus explaining the concomitant occurrence of CBF genetic rearrangements and overexpression of wild type or mutant KIT in AML.
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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.