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    Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein.

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    Authors
    Elzinga, Baukje M
    Nyhan, Michelle J
    Crowley, Lisa C
    O'Donovan, Tracey R
    Cahill, Mary R
    McKenna, Sharon L
    Affiliation
    Leslie C. Quick Laboratory, Cork Cancer Research Centre, BioSciences Institute, University College Cork, Cork, Ireland.
    Issue Date
    2013-06
    MeSH
    Adenine
    Animals
    Apoptosis Regulatory Proteins
    Autophagy
    Benzamides
    Cell Line, Tumor
    Down-Regulation
    Fusion Proteins, bcr-abl
    Gene Knockdown Techniques
    Humans
    K562 Cells
    Leukemia, Myelogenous, Chronic, BCR-ABL Positive
    Membrane Proteins
    Mice
    Phagosomes
    Piperazines
    Proteasome Endopeptidase Complex
    Protein Kinase Inhibitors
    Pyrimidines
    RNA, Small Interfering
    Signal Transduction
    Transfection
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    Citation
    Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein. 2013, 88 (6):455-62 Am. J. Hematol.
    Journal
    American journal of hematology
    URI
    http://hdl.handle.net/10147/322353
    DOI
    10.1002/ajh.23428
    PubMed ID
    23440701
    Additional Links
    http://onlinelibrary.wiley.com/doi/10.1002/ajh.23428/abstract
    Abstract
    Chronic Myeloid Leukemia (CML) is a disease of hematopoietic stem cells which harbor the chimeric gene Bcr-Abl. Expression levels of this constitutively active tyrosine kinase are critical for response to tyrosine kinase inhibitor treatment and also disease progression, yet the regulation of protein stability is poorly understood. We have previously demonstrated that imatinib can induce autophagy in Bcr-Abl expressing cells. Autophagy has been associated with the clearance of large macromolecular signaling complexes and abnormal proteins, however, the contribution of autophagy to the turnover of Bcr-Abl protein in imatinib treated cells is unknown. In this study, we show that following imatinib treatment, Bcr-Abl is sequestered into vesicular structures that co-localize with the autophagy marker LC3 or GABARAP. This association is inhibited by siRNA mediated knockdown of autophagy regulators (Beclin 1/ATG7). Pharmacological inhibition of autophagy also reduced Bcr-Abl/LC3 co-localization in both K562 and CML patient cells. Bcr-Abl protein expression was reduced with imatinib treatment. Inhibition of both autophagy and proteasome activity in imatinib treated cells was required to restore Bcr-Abl protein levels to those of untreated cells. This ability to down-regulate Bcr-Abl protein levels through the induction of autophagy may be an additional and important feature of the activity of imatinib.
    Item Type
    Article
    Language
    en
    ISSN
    1096-8652
    ae974a485f413a2113503eed53cd6c53
    10.1002/ajh.23428
    Scopus Count
    Collections
    Cork University Hospital

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