ArticleBlood2009
Regulation of mir-196b by MLL and its overexpression by MLL fusions contributes to immortalization.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 220 citations in OpenAlex.
- The hidden regulators: Non-coding RNAs in KMT2A-rearranged acute lymphoblastic leukemia.International journal of cancer · 2026Review
- Review
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- Molecular leveraging of HOX-embedded non-coding RNAs in the progression of acute myeloid leukemia.Human cell · 2024Review
- miRNA-7145-cuedc2 axis controls hematopoiesis through JAK1/STAT3 signaling pathway.Cell death discovery · 2024Article
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- MiRNAs in Hematopoiesis and Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2023Review
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- METTL3 Promotes Osteo/Odontogenic Differentiation of Stem Cells by Inhibiting miR-196b-5p Maturation.Stem cells international · 2023Article
- Emerging Roles of Epigenetic Regulators in Maintaining Hematopoietic Stem Cell Homeostasis.Advances in experimental medicine and biology · 2023Article
- Article
- miR-196b-TLR7/8 Signaling Axis Regulates Innate Immune Signaling and Myeloid Maturation in DNMT3A-Mutant AML.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Small-Molecule Inhibitors of the MLL1 CXXC Domain, an Epigenetic Reader of DNA Methylation.ACS medicinal chemistry letters · 2022Article
- Review
- MicroRNA expression is deregulated by aberrant methylation in B-cell acute lymphoblastic leukemia mouse model.Molecular biology reports · 2022Article
- A microRNA signature for clinical outcomes of pediatric ALL patients treated with TPOG protocols.American journal of cancer research · 2022Article
- miR-196b-5p inhibits proliferation of Wharton's jelly umbilical cord stem cells.FEBS open bio · 2021Article
- Expression of microRNA-181a and microRNA-196b in Egyptian Pediatric acute Lymphoblastic Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- The microRNA miR-196b acts as a tumor suppressor in Cdx2-driven acute myeloid leukemia.Haematologica · 2020Article
- High Expression of miR-196b Predicts Poor Prognosis in Patients with Ovarian Cancer.OncoTargets and therapy · 2020Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Chromosomal translocations involving the Mixed Lineage Leukemia (MLL) gene produce chimeric proteins that cause abnormal expression of a subset of HOX genes and leukemia development. Here, we show that MLL normally regulates expression of mir-196b, a hematopoietic microRNA located within the HoxA cluster, in a pattern similar to that of the surrounding 5' Hox genes, Hoxa9 and Hoxa10, during embryonic stem (ES) cell differentiation. Within the hematopoietic lineage, mir-196b is most abundant in short-term hematopoietic stem cells and is down-regulated in more differentiated hematopoietic cells. Leukemogenic MLL fusion proteins cause overexpression of mir-196b, while treatment of MLL-AF9 transformed bone marrow cells with mir-196-specific antagomir abrogates their replating potential in methylcellulose. This demonstrates that mir-196b function is necessary for MLL fusion-mediated immortalization. Furthermore, overexpression of mir-196b was found specifically in patients with MLL associated leukemias as determined from analysis of 55 primary leukemia samples. Overexpression of mir-196b in bone marrow progenitor cells leads to increased proliferative capacity and survival, as well as a partial block in differentiation. Our results suggest a mechanism whereby increased expression of mir-196b by MLL fusion proteins significantly contributes to leukemia development.
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Registered trials
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.