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Gambogic acid-induced autophagy in nonsmall cell lung cancer NCI-H441 cells through a reactive oxygen species pathway


 Department of Respiratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China

Correspondence Address:
Shujun Wang,
Department of Respiratory, The First Affiliated Hospital of Zhengzhou University, No. 1, Jianshedong Road, Zhengzhou 450052
China
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Source of Support: None, Conflict of Interest: None

Aim of the Study: Garcinia hanburyi is a traditional herbal medicine with activities of anti-inflammation and hemostasis used by people in South Asia. Gambogic acid (GA) is the main active component extracted from it, which has anticancer and anti-inflammatory effects. The aim of the current study is to investigate the molecular mechanisms of GA's effective anticancer activity. Materials and Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to measure cell proliferation. Apoptosis induced by GA was analyzed by flow cytometry. In addition, monodansylcadaverine (MDC) and 2',7'-dichlorofluorescein diacetate were used to evaluate autophagy and reactive oxygen species (ROS) generation, respectively. Results: GA could significantly inhibit nonsmall cell lung cancer (NSCLC) NCI-H441 cell growth. In addition, GA induced NCI-H441 cells autophagy, confirmed by MDC staining, upregulation of Beclin 1 (initiation factor for autophagosome formation), and conversion of LC3 I to LC3 II (autophagosome marker). Moreover, generated ROS was induced by GA in NCI-H441 cells and the ROS scavenger N-acetylcysteine reversed GA-induced autophagy and restored the cell survival, which indicated GA-induced autophagy in NCI-H441 cells through an ROS-dependent pathway. In addition, in vivo results further indicated that GA significantly inhibited the growth of NCI-H441 xenografts. Conclusion: The results shed new light on the interaction between ROS generation and autophagy in NSCLC cells and provide theoretical support for the usage of GA in clinical treatment.


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    -  Ye L
    -  Zhou J
    -  Zhao W
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