ArticleHaematologica2015
Pbx3 and Meis1 cooperate through multiple mechanisms to support Hox-induced murine leukemia.
Article in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- The diverse roles of Hox proteins in the regulation of the cell cycle and their therapeutic value in cancer treatment.Cancer metastasis reviews · 2026Review
- The P2X7 receptor in leukemia: pathological mechanisms and therapeutic potential.Purinergic signalling · 2025Review
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- High NUP210 mRNA expression and its role in prognosis of acute myeloid leukemia.Clinical and experimental medicine · 2025Article
- Pbx3-mediated suppression of type I interferon response contributes to leukemia progression driven by MLL-AF9.Cancer gene therapy · 2025Article
- The role of tribbles homolog 2 in cell proliferation.Cell communication and signaling : CCS · 2025Review
- Menin inhibitors for the treatment of acute myeloid leukemia: challenges and opportunities ahead.Journal of hematology & oncology · 2024Review
- Low expression of miR-182 caused by DNA hypermethylation accelerates acute lymphocyte leukemia development by targeting PBX3 and BCL2: miR-182 promoter methylation is a predictive marker for hypomethylation agents + BCL2 inhibitor venetoclax.Clinical epigenetics · 2024Article
- Single-cell analysis of shared signatures and transcriptional diversity during zebrafish development.Developmental cell · 2023Article
- The MLL-Menin Interaction is a Therapeutic Vulnerability inHemaSphere · 2023Article
- Single-cell analysis of shared signatures and transcriptional diversity during zebrafish development.bioRxiv : the preprint server for biology · 2023Article
- Developmentally regulated expression of integrin alpha-6 distinguishes neural crest derivatives in the skin.Frontiers in cell and developmental biology · 2023Article
- In toto imaging of early enteric nervous system development reveals that gut colonization is tied to proliferation downstream of Ret.Development (Cambridge, England) · 2022Article
- Meis1 supports leukemogenesis through stimulation of ribosomal biogenesis and Myc.Haematologica · 2022Article
- Transcription factor Meis1 act as a new regulator of ischemic arrhythmias in mice.Journal of advanced research · 2022Article
- MEIS1 in Hematopoiesis and Cancer. How MEIS1-PBX Interaction Can Be Used in Therapy.Journal of developmental biology · 2021Review
- MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021Review
- A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene.PLoS genetics · 2021Article
- LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit.Cell death & disease · 2021Article
- Disruption of CTCF Boundary at HOXA Locus Promote BET Inhibitors' Therapeutic Sensitivity in Acute Myeloid Leukemia.Stem cell reviews and reports · 2020Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hox homeobox transcription factors drive leukemogenesis efficiently only in the presence of Meis or Pbx proteins. Here we show that Pbx3 and Meis1 need to dimerize to support Hox-induced leukemia and we analyze the molecular details of this cooperation. In the absence of Pbx3, Meis1 was highly unstable. As shown by a deletion analysis Meis1 degradation was contingent on a motif coinciding with the Pbx-binding domain. Either deletion of this sequence or binding to Pbx3 prolonged the half-life of Meis1 by preventing its ubiquitination. Meis1 break-down could also be blocked by inhibition of the ubiquitin proteasome system, indicating tight post-transcriptional control. In addition, Meis1 and Pbx3 cooperated genetically as overexpression of Pbx3 induced endogenous Meis1 transcription. These functional interactions translated into in vivo activity. Blocking Meis1/Pbx3 dimerization abrogated the ability to enhance proliferation and colony-forming cell numbers in primary cells transformed by Hoxa9. Furthermore, expression of Meis1 target genes Flt3 and Trib2 was dependent on Pbx3/Meis1 dimerization. This correlated with the requirement of Meis1 to bind Pbx3 in order to form high affinity DNA/Hoxa9/Meis1/Pbx3 complexes in vitro. Finally, kinetics and severity of disease in transplantation assays indicated that Pbx3/Meis1 dimers are rate-limiting factors for Hoxa9-induced leukemia.
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