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Butein induces EC109 cell apoptosis via activating AMP-activated protein kinase/forkhead class box O3a pathway and cellular oxidative stress |
CHEN Shaoyang YUE Honglin LIU Xu |
Intensive Care Unit, 263 Clinical Department, Army General Hospital, Beijing 101149, China |
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Abstract Objective To investigate the effects of Butein on esophagus cancer EC109 cells and the role of AMP-activated protein kinase (AMPK)/forkhead class box O3a (FOXO3a) and oxidative stress in this process. Methods EC109 cell was routine cultured and given Butein, the cell vitality, migration ability, cellular oxidative stress level of EC109 cell and Caspase 3 activity were detected. The AMPK, FOXO3 aphosphorylation level and the expressions of Bim and Bax were detected by Western blot. After Compound C inhibit AMPK, related indicators were detected. The nude mice tumor bearing model was made, Butein and Compound C were given, the weight and tumor volume of nude mice were detected. Results After Butein treatment, cell vitality reduced, the distance between cell boundaries increased, ROS concentration and NADPH oxidase activity increased, total GSH level and Caspase 3 activity reduced (P < 0.05); AMPKand FOXO3 aphosphorylation and cell apoptosis increased (P < 0.05); Compound C treatment reversed this process. The nude mice tumor study showed that Butein inhibited the tumor growth and Compound C reversed this effect. Conclusion Butein can induce EC109 cell apoptosis, and this process may be mediated by activation of AMPK/FOXO3a and cellular oxidative stress.
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