KO-HSIU LU2026-10-162026-10-162005-07-01Pure ID: 15361457Pure UUID: d43f252b-73b6-4f47-a726-30ae7306c56e10.1016/j.cccn.2005.02.003https://www.scopus.com/pages/publications/20444452899https://scholars.csmu.edu.tw/handle/123456789/32665Background: 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.9enjournal article