Induction of caspase-3-dependent apoptosis in human leukemia HL-60 cells by paclitaxel.

doi:10.1016/j.cccn.2005.02.003

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/10537

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題名:	Induction of caspase-3-dependent apoptosis in human leukemia HL-60 cells by paclitaxel.
作者:	Lu KH Lue KH Liao HH Lin KL Chung JG
貢獻者:	中山醫學大學
關鍵詞:	Paclitaxel;HL-60 cells;Cell cycle;Apoptosis;Caspase-3
日期:	2005-07
上傳時間:	2015-03-23T04:30:34Z (UTC)
ISSN:	0009-8981
摘要:	BACKGROUND: Paclitaxel, an antineoplastic drug, inhibits cell growth and cell cycle progression and induces apoptosis in human leukemia HL-60 cells. Caspase-3 plays a direct role in proteolytic cleavage of cellular proteins responsible for progression to apoptosis. METHODS: We examined the cell morphology and apoptosis in HL-60 cells after exposure to paclitaxel and measured caspase-3 activities with or without z-VAD-fmk (a broad-spectrum caspase inhibitor) pretreatment by flow cytometric analysis and Western blotting. RESULTS: Together, our results were (1) paclitaxel mainly induced G2/M cell cycle arrest in HL-60 cells (p<0.001); (2) time (p<0.001)- and dose-dependent (p<0.001) apoptosis of HL-60 cells was induced by paclitaxel; (3) in HL-60 cells, z-VAD-fmk blocked paclitaxel-induced apoptosis (12 h: p<0.001; 24 h: p<0.01; 48 h: p<0.01; 72 h: p<0.001) and caspase-3 activation (12 h: p<0.05; 24 h: p<0.01; 48 h: p<0.01; 72 h: p<0.01). CONCLUSIONS: These results suggest that paclitaxel can induce G2/M cell cycle transition and apoptosis via caspase-3 activity in HL-60 cells.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10537 http://dx.doi.org/10.1016/j.cccn.2005.02.003
關聯:	Clin Chim Acta. 2005 Jul 1;357(1):65-73.
顯示於類別:	[醫學系] 期刊論文

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