Abstract
In this study, the anti-proliferative effect of physcion, an anthraquinone derivative isolated and characterized from both terrestrial and marine sources, against human gastric cancer SGC-7901 cells was investigated and the underlying mechanisms were explored. Physcion reduced SGC-7901 cell viability in a dose- and time-dependent manner, as demonstrated by MTT assay. It triggered the mitochondrial/caspase apoptotic pathway indicated by loss of mitochondrial membrane potential and cytochrome c release. Moreover, physcion induced a sustained activation of the phosphorylation of AMPK, and compound C (an inhibitor of AMPK) significantly reversed physcion-induced apoptosis in SGC-7901 cells. In addition, physcion provoked the generation of reactive oxygen species (ROS) in SGC-7901 cells, while the antioxidant N-acetyl cysteine almost completely blocked physcion-induced AMPK activation and apoptosis. Taken together, these findings suggest that physcion induces apoptosis through a ROS/AMPK-dependent mitochondrial pathway.
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