文化大學機構典藏 CCUR:Item 987654321/20512
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://irlib.pccu.edu.tw/handle/987654321/20512


    题名: Oral small-molecule tyrosine kinase inhibitor midostaurin (PKC412) inhibits growth and induces megakaryocytic differentiation in human leukemia cells
    作者: Huang, YC (Huang, Yu-Chuen)
    Chao, DK (Chao, David K.)
    Chao, KSC (Chao, K. S. Clifford)
    Chen, YJ (Chen, Yu-Jen)
    贡献者: 運動教練研究所
    关键词: Megakaryocyte
    Differentiation
    Midostaurin
    PKC412
    Apoptosis
    日期: 2009
    上传时间: 2011-11-30 12:40:31 (UTC+8)
    摘要: Midostaurin (PKC412), a small-molecule multiple tyrosine kinase inhibitor, has been shown to suppress the growth of various tumor cells. Since kinases inhibited by midostaurin are involved in megakaryocytic differentiation, we hypothesized that this novel target therapeutic might have a role in the treatment of human leukemia cells. Hence, we examined the effect of midostaurin on human erythroleukemia cells and evaluated potential mechanisms. Midostaurin inhibited the growth of both K562 and HEL cells in dose- and time-dependent manner. Morphological changes such as enlarged contours, multipolarity of mitotic spindles, and multinucleation of megakaryocytes were noted in both cell lines treated by midostaurin. A smaller population of apoptotic cells was also observed. DNA histogram revealed polyploid and hypoploid populations of midostaurin-treated cells. Midostaurin treatment enhanced the surface expression of the megakaryocytic marker CD61: in contrast. the erythroid marker glycophorin A expression was decreased. At optimal conditions for inducing megakaryocytic differentiation, midostaurin upregulated the expression and signaling of c-Mpl. a thrombopoietin receptor-encoding gene, in HEL cells. These results indicate that midostaurin can inhibit growth; induce megakaryocytic differentiation; and to a lesser extent, cause apoptosis in HEL cells. This effect might involve the expression and signaling of c-Mpl. (C) 2009 Elsevier Ltd. All rights reserved.
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