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Ginsenoside Rk1 induces cell cycle arrest and apoptosis in MDA-MB-231 triple negative breast cancer cells
- Hong, Yinan, Fan, Daidi
- Toxicology 2019 v.418 pp. 22-31
- Panax, Western blotting, acetylcysteine, antineoplastic activity, antineoplastic agents, apoptosis, breast neoplasms, caspase-3, cell cycle checkpoints, cell proliferation, enzyme inhibitors, ginsenosides, insulin, interphase, membrane potential, mitochondrial membrane, models, neoplasm cells, reactive oxygen species, toxicity
- Ginsenoside Rk1 (Rk1) is a component found in processed ginseng that exhibits anti-insulin resistance, anti-inflammation and anti-cancer activities. However, there are few reports of Rk1 activity against triple negative breast cancer (TNBC). In this study, the anti-proliferation and potential mechanisms of Rk1 in MDA-MB-231 cells were investigated. Xenograft model exhibited that Rk1 significantly repressed tumor growth with low toxicity to major organs. Moreover, Rk1 dramatically inhibited cell proliferation, colony formation, promoted LDH release, and induced G0/G1 phase arrest. Rk1 also triggered intracellular reactive oxygen species (ROS) generation and mitochondrial membrane potential reduction. Western blot results revealed that Rk1 increased the expression of Bax, cytochrome C, cleaved caspase 3, 8 and 9 levels and decreased Bcl-2 level and blocked the PI3K/Akt pathway. Pretreatment with the pan-caspase inhibitor Z-VAD-FMK, PI3K/Akt pathway activator insulin or ROS scavenger N-acetylcysteine (NAC) further demonstrated that ROS/PI3K/Akt pathway was responsible for Rk1-induced apoptosis. Overall, this is the first study to illustrate the anti-triple negative breast cancer effects and mechanisms of Rk1 and ginsenoside Rk1 could be a new promising anti-tumor drug for TNBC.