Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
Volume 13, Issue 6, Pages 782-793Publisher
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.18732
Keywords
gallbladder cancer; apoptosis; dioscin; reactive oxygen species
Categories
Funding
- National Natural Science Foundation of China [81572819, 81172026, 81272402, 81301816, 81172029, 81402403, 81502433, 31501127]
- China Postdoctoral Science Foundation [2015M571577]
- Program for Changjiang Scholars
- Natural Science Research Foundation of Shanghai Jiao Tong University School of Medicine [13XJ10037]
- Leading Talent program of Shanghai [20130073130014]
- Interdisciplinary Program of Shanghai Jiao Tong University [14JCRY05]
- Shanghai Rising-Star Program [15QA1403100]
- Specialized Research Foundation for the PhD Program of Higher Education-Priority Development Field [20130073130014]
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Gallbladder cancer (GBC), highly aggressive form of cancer with an extremely poor prognosis, is the most common malignancy of the biliary tract. In this study, we investigated the effects of dioscin (DSN) on human GBC and the potential mechanisms underlying these effects. The results showed that DSN significantly inhibited GBC cell proliferation and migration. Moreover, DSN induced GBC cell apoptosis via mitochondrial dependent apoptotic signalling. Reactive oxygen species (ROS) and glutathione (GSH) levels were measured, and ROS scavengers completely inhibited DSN-induced apoptosis and migration, indicating that ROS play an essential role in GBC progression. Western blot analysis showed that AKT activity was significantly downregulated after DSN treatment, and that inhibition/ectopic expression of AKT enhanced/abolished DSN-induced apoptosis but not migration. Furthermore, we confirmed the relationship between ROS and the PI3K/AKT pathway and found that DSN induced apoptosis by regulating ROS-mediated PI3K/AKT signaling. Taken together, these findings indicate that DSN induces GBC apoptosis through inhibiting ROS-mediated PI3K/AKT signalling.
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