https://scholars.lib.ntu.edu.tw/handle/123456789/470507
標題: | Beauvericin induces cytotoxic effects in human acute lymphoblastic leukemia cells through cytochrome c release, caspase 3 activation: The causative role of calcium | 作者: | Jow, Guey Mei Chou, Cheng Jen Chen, Bing Fang JIA-HUEI TSAI |
關鍵字: | Apoptosis | Beauvericin | Calcium | Caspase-3 | Cytochrome c | 公開日期: | 28-十二月-2004 | 出版社: | ELSEVIER IRELAND LTD | 卷: | 216 | 期: | 2 | 起(迄)頁: | 165 | 來源出版物: | Cancer Letters | 摘要: | Beauvericin (BEA), a cyclic hexadepsipeptide, induces cell death in human leukemia cells (CCRF-CEM) and the process of BEA-induced cell death has been speculated to undergo an apoptotic pathway. In the present study, several well-characterized factors, known to play important roles in apoptotic pathway, were investigated in BEA-induced CCRF-CEM cell death. CCRF-CEM cells were treated with BEA at concentrations from 1 to 10 μM for up to 24 h. The incidence of nuclear fragmentation and apoptotic body formation in the cells, cytosolic caspase-3 activity, mitochondrial membrane potential, and release of cytochrome c (Cyt c) from mitochondria in BEA-treated cells were determined and compared with that in untreated cells. Moreover, to investigate the role of intracellular Ca ++ in this cell death process, CCRF-CEM cells were primed with 3 μM of BAPTA/AM, a Ca ++ chelator, to exclude intracellular Ca ++ prior to the BEA treatment. The data revealed that BEA-induced cell death in CCRF-CEM cells exhibited a dose- and time-dependent manner. The incidence of nuclear fragmentation and apoptotic body formation was significantly increased in CCRF-CEM cells treated with BEA at concentrations of 1 μM or greater. Increase of cytosolic caspase-3 activity was also observed in BEA-treated cells with a dose-dependent manner. In addition, increased release of Cyt c from mitochondria was also observed in the cells treated with 10 μM BEA in a time-dependent pattern. The BAPTA/AM pretreatment partially blocked BEA-induced cell death in CCRF-CEM cells, indicating that intracellular Ca ++ plays an important role, maybe as a mediator in cell death signaling, in this cell death pathway. The results support the notion that BEA-induced cell death in CCRF-CEM cells likely undergo through an apoptotic pathway on the basis of increase of release of Cyt c from mitochondria, increase of caspase-3 activity, and some observed typical apoptotic cellular changes in morphology. © 2004 Elsevier Ireland Ltd. All rights reserved. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/470507 | ISSN: | 03043835 | DOI: | 10.1016/j.canlet.2004.06.005 |
顯示於: | 病理學科所 |
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