| 4-aminopyridine Induces Apoptosis of Human Acute Myeloid Leukemia Cells via Increasing [Ca](i) Through P(2)X(7) Receptor Pathway. | |
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MedLine Citation:
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PMID: 21865727 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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4-AP, a voltage-gated potassium channel blocker, was identified to exert critical pro-apoptotic properties in various types of cancer cells. The present study aims to explore the effect of 4-AP on the apoptosis of human AML cells and the underlying mechanism. We found 4-AP inhibited the proliferation and induces apoptosis in both AML cell lines and primary cultured human AML cells. The apoptosis of AML cells after 4-AP treatment was further confirmed by the disruption of mitochondrial membrane potential (MMP) and activation of caspase 3 and 9. 4-AP inhibited Kv currents in NB(4), HL-60 and THP-1 cells. Furthermore, 4-AP induced significant increment in [Ca(2+)](i), which were inhibited by KN-62, a specific blocker of P(2)X(7) receptors. KN-62 also abrogated 4-AP induced apoptosis. Knockdown of P(2)X(7) receptor by small interfering RNA blocked the effect of 4-AP. Conclusively, this study indicated that 4-AP promotes apoptosis in human AML cells via increasing [Ca(2+)](i) through P(2)X(7) receptor. |
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Authors:
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Wei Wang; Jianbing Xiao; Masaaki Adachi; Zhiyu Liu; Jin Zhou |
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Publication Detail:
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Type: Journal Article Date: 2011-08-16 |
Journal Detail:
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Title: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology Volume: 28 ISSN: 1421-9778 ISO Abbreviation: Cell. Physiol. Biochem. Publication Date: 2011 |
Date Detail:
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Created Date: 2011-08-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9113221 Medline TA: Cell Physiol Biochem Country: Switzerland |
Other Details:
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Languages: eng Pagination: 199-208 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 S. Karger AG, Basel. |
Affiliation:
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Department of Hematology, the First Affiliated Hospital of Harbin Medical University, Harbin, P.R. China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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