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    Regulation of Trib2 by an E2F1-C/EBPα feedback loop in AML cell proliferation.

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    Authors
    Rishi, Loveena
    Hannon, Maura
    Salomè, Mara
    Hasemann, Marie
    Frank, Anne-Katrine
    Campos, Joana
    Timoney, Jennifer
    O'Connor, Caitriona
    Cahill, Mary R
    Porse, Bo
    Keeshan, Karen
    Show allShow less
    Affiliation
    Paul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland;
    Issue Date
    2014-04-10
    MeSH
    3T3 Cells
    Animals
    CCAAT-Enhancer-Binding Proteins
    Cell Proliferation
    Cell Transformation, Neoplastic
    Chromatin Immunoprecipitation
    E2F1 Transcription Factor
    Electrophoretic Mobility Shift Assay
    Feedback, Physiological
    Gene Expression Regulation, Neoplastic
    Humans
    Intracellular Signaling Peptides and Proteins
    Leukemia, Myeloid, Acute
    Mice
    Mice, Inbred C57BL
    Mice, Knockout
    Protein-Serine-Threonine Kinases
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    Citation
    Regulation of Trib2 by an E2F1-C/EBPα feedback loop in AML cell proliferation. 2014, 123 (15):2389-400 Blood
    Journal
    Blood
    URI
    http://hdl.handle.net/10147/322364
    DOI
    10.1182/blood-2013-07-511683
    PubMed ID
    24516045
    Additional Links
    http://bloodjournal.hematologylibrary.org/content/123/15/2389.long?sso-checked=1
    Abstract
    The loss of regulation of cell proliferation is a key event in leukemic transformation, and the oncogene tribbles (Trib)2 is emerging as a pivotal target of transcription factors in acute leukemias. Deregulation of the transcription factor E2F1, normally repressed by CCAAT enhancer-binding protein α (C/EBPα)-p42, occurs in acute myeloid leukemia (AML), resulting in the perturbation of cell cycle and apoptosis, emphasizing its importance in the molecular pathogenesis of AML. Here we show that E2F family members directly regulate Trib2 in leukemic cells and identify a feedback regulatory loop for E2F1, C/EBPα, and Trib2 in AML cell proliferation and survival. Further analyses revealed that E2F1-mediated Trib2 expression was repressed by C/EBPα-p42, and in normal granulocyte/macrophage progenitor cells, we detect C/EBPα bound to the Trib2 promoter. Pharmacological inhibition of the cell cycle or Trib2 knockdown resulted in a block in AML cell proliferation. Our work proposes a novel paradigm whereby E2F1 plays a key role in the regulation of Trib2 expression important for AML cell proliferation control. Importantly, we identify the contribution of dysregulated C/EBPα and E2F1 to elevated Trib2 expression and leukemic cell survival, which likely contributes to the initiation and maintenance of AML and may have significant implications for normal and malignant hematopoiesis.
    Item Type
    Article
    Language
    en
    ISSN
    1528-0020
    ae974a485f413a2113503eed53cd6c53
    10.1182/blood-2013-07-511683
    Scopus Count
    Collections
    Cork University Hospital

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