Ginsenoside Rk1 Induced Apoptosis in Ovarian Cancer SK-OV-3 Cells via ROS-Mediated Caspase Signaling Pathway

Background and Objective: Ovarian cancer has the highest mortality rate of all gynecologic cancers, exploring natural plant-derived antitumor drugs has become indispensable in ovarian cancer treatment. Ginsenoside Rk1 exerted numerous pharmacological activities including anti-tumour and anti-inflammation. The present study explored the effect of ginsenoside Rk1 (G-Rk1) on the proliferation and apoptosis in SK-OV-3 ovarian cancer cells and deepened its mechanism of action. Materials and Methods: Cell viability was measured by MTT assay. Changes in mitochondrial membrane potential (MMP) and Hoechst 33258 staining were used to detect cell apoptosis. Western blot was used to detect the release of cytochrome C and expression of apoptosis-related proteins Bcl-2, Bax and cleaved caspase-3, cleaved caspase-9. Additionally, flow cytometry was used to detect cellular cycles and apoptosis. Results: The G-Rk1 significantly inhibited cell viability dose-dependently (p<0.01). In addition, G-Rk1-induced apoptosis was investigated through reactive oxygen species (ROS) and mitochondrial membrane potential loss. It was observed that G-Rk1 can not only induce cell cycle arrest at the G1 phase but also inhibit the proliferation ability of SK-OV-3 cells. Importantly, western blot analysis confirmed that more cytochrome c was released from mitochondria resulting in caspase activation (p<0.05). Conclusion: Therefore, the findings from the present study exhibited that G-Rk1 could inhibit the proliferation of SK-OV-3 ovarian cancer cells and maybe as a candidate drug for anti-ovarian cancer soon.