Objective: To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods: Cell growth inhibition of paclitaxel on A549 cells was analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst33258 staining when treated with paclitaxel for 48 hours. Meanwhile, Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results: Paclitaxel inhibited the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 11.52 ± 1.94%,17.73 ± 2.53%, and 29.32 ± 5.51% respectively, which were significantly higher than those of control group 5.88 ± 1.07%(all P﹤0.01), and apoptosis rate increased in dose-dependant manner. Meanwhile, G2/M stage cell percentage of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 42.52 ± 6.25%, 40.46 ± 5.81%, and 35.34 ± 6.17% respectively,which were significantly higher than that of control group 22.32 ± 3.30%(all P﹤0.01); Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependant manner. Conclusion: Paclitaxel can inhibit A549 cell proliferation in a time- and dose-dependant manner. Its mechanism may be related to arresting cell cycle in G2/M stage and induce cell apoptosis by up-modulating Bax expression and down-modulating Bcl-2 expression. Objective: To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods: Cell growth inhibition of paclitaxel on A549 cells were analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst 33258 staining when treated with paclitaxel for 48 hours. Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results: Paclitaxel inhibited the proliferation of A549 cells in a time -and dose-dependent manner. Hoechst 33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmol / L, 50 nmol / L and 100 nmol / L paclitaxel groups were 11.52 ± 1.94%, 17.73 ± 2.53%, and 29.32 ± 5.51% respectively, which were significantly higher than those of control group 5.88 ± 1.07% (all P <0.01), and apoptosis rate increased in dose-dependent manner. Meanwhile, G2 / M stage cell percentage of 25 nmol / L, 50 nmol / L and 100 nmol / L paclitaxel groups were 42.52 ± 6.25%, 40.46 ± 5.81%, and 35.34 ± 6.17% respectively, which were significantly higher than that of control group 22.32 ± 3.30% (all P <0.01); Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependent manner. Conclusion: Paclitaxel can inhibit A549 cell proliferation in a time- and dose-dependent manner. Its mechanism may be related to arresting cell cycle in G2 / M stage and induce cell apoptosis by up-modulating Bax expression and down-modulating Bcl-2 expression.