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 310902500/18151

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题名:	Induction of caspase-3-dependent apoptosis in human leukemia HL-60 cells by paclitaxel
作者:	Lu, K.-H.;Lue, K.-H.;Liao, H.-H.;Lin, K.-L.;Chung, J.-G.
关键词:	Apoptosis;Caspase-3;Cell cycle;HL-60 cells;Paclitaxel
日期:	2005
上传时间:	2017-08-07T09:14:56Z (UTC)
ISSN:	98981
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. ? 2005 Elsevier B.V. All rights reserved.
URI:	http://dx.doi.org/10.1016/j.cccn.2005.02.003 https://www.scopus.com/inward/record.uri?eid=2-s2.0-20444452899&doi=10.1016%2fj.cccn.2005.02.003&partnerID=40&md5=4df2082dd761860347914f050000657f https://ir.csmu.edu.tw:8080/ir/handle/310902500/18151
關聯:	Clinica Chimica Acta 357(1),65-73
显示于类别:	[醫學系] 期刊論文

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