Abstract: BACKGROUND AND AIM: To assess the growth-inhibiting effects of paclitaxel on p53-deficient human lung cancer H1299 cell line in vitro. MATERIALS AND METHODS: H1299 cells were exposed to paclitaxel at different concentrations or different treatment times, then the growth-inhibiting effects were determined by MTT assay, the change of the cell cycle and apoptosis were analyzed with flow cytometry. Fluorescence microscopy was used to observe the nucleolus change stained by Hoechst33342 and PI. RESULTS: The growth inhibition effect of paclitaxel on H1299 cells was time-dependent(P<0.05). With treatment concentration>1 nmol/L, the survival rate of H1299 cells in paclitaxel-treated groups decreased with increasing paclitaxel concentration, and showing significant difference with the survival rate in control group (P<0.05). The H1299 cells treated by 0.1－1 000 nmol/L paclitaxel were blocked at G2/M phase, and the percentage of G2/M phase increased in concentration-dependent manner. The proportion of apoptosis increased as concentration changed from 0 to 10 nmol/L(P<0.05). The induction of apoptosis was time dependent(P<0.05) and the percentage of G2/M phase was highest at 12 h with paclitaxel at 10 nmol/L. When treated with 1 000 nmol/L paclitaxel, H1299 showed the highest G2/M arrest at 24 h and some polyploidy cells appeared with prolonged treatment. Both concentrations could induce time-dependent apoptosis, but the higher concentration caused apoptosis later than the lower one. Apoptosis had no relationship with G2/M arrest(P>0.05). The coexistence of cell apoptosis and necrosis could be observed in paclitaxel-treated H1299 cells under fluorescence microscopy. CONCLUSION: Paclitaxel could induce apoptosis and necrosis of H1299 at the same time. It inhibited the growth of H1299 cells in vitro in time-and concentration-dependent manners.

Key words: lung neoplasms, paclitaxel, apoptosis, cell cycle