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.
