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

CMUR > College of Life Sciences > Department of Biological Science and Technology > Journal articles > Item 310903500/6260

Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/6260

Title:	Induction of caspase-3-dependent apoptosis in human leukemia HL-60 cells by paclitaxel.
Authors:	(Lu KH)、(Lue KH)、(Liao HH)、(Lin KL)、鍾景光(Jing-Gung Chung)*
Contributors:	生命科學院生物科技學系;中國附醫醫學研究部
Keywords:	Paclitaxel;HL-60 cells;Cell cycle;Apoptosis;Caspase-3
Date:	2005.07
Issue Date:	2009-08-25 14:39:32 (UTC+8)
Abstract:	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 b0.001); (2) time ( p b0.001)- and dose-dependent ( p b0.001) apoptosis of HL-60 cells was induced by paclitaxel; (3) in HL-60 cells, z-VADfmk blocked paclitaxel-induced apoptosis (12 h: p b0.001; 24 h: p b0.01; 48 h: p b0.01; 72 h: p b0.001) and caspase-3 activation (12 h: p b0.05; 24 h: p b0.01; 48 h: p b0.01; 72 h: p b0.01). Conclusions: These results suggest that paclitaxel can induce G2/M cell cycle transition and apoptosis via caspase-3 activity in HL-60 cells.
Relation:	CLINICA CHIMICA ACTA 357(1 )65 ~73
Appears in Collections:	[Department of Biological Science and Technology] Journal articles

Files in This Item:

File	Size	Format
	0Kb	Unknown	425	View/Open

Loading...