Ginsenoside F2 induces apoptosis in humor gastric carcinoma cells through reactive oxygen species-mitochondria pathway and modulation of ASK-1/JNK signaling cascade in vitro and in vivo

Ginsenoside F2 (F2) is a potential bioactive metabolite of major ginsenosides. The potential anti-cancer effect of F2 in gastric cancer cells has not been appraised. This study investigated the effects of F2 on the production of reactive oxygen species (ROS). We also investigated the in vitro and in vivo effects of F2 on the downstream signaling pathways leading to apoptosis in human gastric cancer cells. The in vitro data revealed that F2 induces ROS accumulation followed by a decrease in mitochondrial transmembrane potential (MTP), and the release of cytochrome c (cyto c), which induced the caspase-dependent apoptosis. Further assay indicated that modulation of ASK-1/JNK pathway contributes to apoptosis. In vivo, F2 exhibits the obvious anti-cancer effect compared with cisplatin with no obvious toxicity. Jointly, these results suggest that F2 induces apoptosis by causing an accumulation of ROS and activating the ASK-1/JNK signaling pathway. This provides further support for the use of F2 as a novel anticancer therapeutic candidate.

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