Effects of Paclitaxel on Cell Proliferation and Apoptosis of Human Lung Adenocarcinoma A549 Cells
Jun Yang
Abstract
Jun Yang
Abstract
Objective: To investigate the effects 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 Hoechst 33258 staining after paclitaxel treatment for 48 hours. Cell cycle and apoptotic rate were analyzed by cytometry. Protein expressions of Bax and Bcl-2 were studied by Western Blot. Results: Paclitaxel could inhibit the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst 33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours,G2~M stage cell percentage of paclitaxel groups were significantly higher than that of control group(P 0.01). Cell apoptosis rate of paclitaxel groups were significantly higher than that of control group(P 0.01). And apoptosis rate increased in dose-dependant manner. Western blot showed that paclitaxel increased protein express of Bax and decreased protein express of Bcl-2 in a dose-dependant manner. Conclusion: Paclitaxel can inhibit A549 cells proliferation in a time- and dose-dependant manner. The mechanism may be to arrest cell cycle in G2~M stage and induce cell apoptosis by upmodulating Bax expression and downmodulating Bcl-2 expression.
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Objective: To investigate the effects 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 Hoechst 33258 staining after paclitaxel treatment for 48 hours. Cell cycle and apoptotic rate were analyzed by cytometry. Protein expressions of Bax and Bcl-2 were studied by Western Blot. Results: Paclitaxel could inhibit the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst 33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours,G2~M stage cell percentage of paclitaxel groups were significantly higher than that of control group(P 0.01). Cell apoptosis rate of paclitaxel groups were significantly higher than that of control group(P 0.01). And apoptosis rate increased in dose-dependant manner. Western blot showed that paclitaxel increased protein express of Bax and decreased protein express of Bcl-2 in a dose-dependant manner. Conclusion: Paclitaxel can inhibit A549 cells proliferation in a time- and dose-dependant manner. The mechanism may be to arrest cell cycle in G2~M stage and induce cell apoptosis by upmodulating Bax expression and downmodulating Bcl-2 expression.
Key concepts: Apoptosis, Paclitaxel, A549 cell, Cell cycle, Cell growth, Western blot, MTT assay, Cell