| Bortezomib and sphingosine kinase inhibitor interact synergistically to induces apoptosis in BCR/ABl(+) cells sensitive and resistant to STI571 through down-regulation Mcl-1. | |
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MedLine Citation:
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PMID: 21195056 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Interactions between the proteasome inhibitor, bortezomib, and the sphingosine kinase (SPK1) inhibitor, SKI, were examined in BCR/ABL human leukemia cells. Coexposure of K562 or chronic myeloid leukemia (CML) cells from patients to subtoxic concentrations of SKI (10μM) and bortezomib (100nM) resulted in a synergistic increase in caspase-3 cleavage and apoptosis. These events were associated with the downregulation of BCR-ABL and Mcl-1, and a marked reduction in SPK1 expression. In imatinib mesylate-resistant K562 cells that displayed decreased BCR-ABL expression, bortezomib/SKI treatment markedly increased apoptosis and inhibited colony-formation in association with the downregulation of Mcl-1. Finally, the bortezomib/SKI regimen also potently induced the downregulation of BCR/ABL and Mcl-1 in human leukemia cells. Collectively, these findings suggest that combining SKI and bortezomib may represent a novel strategy in leukemia, including apoptosis-resistant BCR-ABL(+) hematologic malignancies. |
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Authors:
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Qing-Fang Li; Jun Yan; Kai Zhang; Yue-Feng Yang; Feng-Jun Xiao; Chu-Tse Wu; Hua Wang; Li-Sheng Wang |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2010-12-30 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: - ISSN: 1090-2104 ISO Abbreviation: - Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2011-1-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Experimental Hematology, Beijing Institute of Radiation Medicine, 27 Taiping Road, Beijing 100850, PR China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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