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| Butein exerts pro-apoptotic activity in lung adenocarcinoma A549 cells via the regulation of STAT3 signaling |
| CHEN Shaoyang YUE Honglin LIU Xu |
| Department of Intensive Care Unit, 263 Clinical Department, Army General Hospital, Beijing 101149, China |
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Abstract Objective To investigate the pro-apoptotic effect of Butein (BTN) in lung adenocarcinoma A549 cells and the role of STAT3 signaling in this process. Methods A549 cells were cultured and treated with different concentrations of BTN (0, 25, 50 μmol/L) for 24 h. BTN 0 μmol/L was taken as the control group. The survival rate, apoptotic rate, cell migration, ROS generation, Caspase-3 activity were respectively detected after treatment. Western blot was used to detect expression of p-STAT3, STAT3, Bcl-2 and Bax. NAC 5 mmol/L was used to block the generation of ROS, then BTN treatment (0, 50 μmol/L) was implemented for further detection as mentioned. Besides, in vivo studies were also used to verify whether abdominal injection with BTN (2, 4 mg/kg) exerted anticancer activity, while the control group was injected with PBS. Results Compared with the control group, BTN (25, 50 μmol/L) treatment resulted in reduction of cell viability and migration (P < 0.05), promotion of cell apoptosis (P < 0.05), up-regulation of ROS and Caspase-3 levels (P < 0.05). BTN treatment resulted in a significant down-regulation of p-STAT3 and Bcl-2, and up-regulation of Bax (P < 0.05). Moreover, inhibition of ROS by NAC antagonized the anti-STAT3 phosphorylated and pro-apoptotic role of BTN on A549 cells (P < 0.05). In vivo studies showed that compared the control group, tumor volume and p-STAT3 expression in nude mice were significantly reduced after BTN treatment (P < 0.05). Conclusion BTN treatment effectively inhibits cell viability and promotes apoptosis in A549 cells, which may be related to the up-regulation of ROS level thus inhibiting STAT3 phosphorylation.
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