Purpose
We tried to clarify the cytotoxic mechanism of VK3 using the breast cancer cell line MCF-7.
Methods
Cytotoxicity was measured via intracellular esterase activity. DNA fragmentation was assessed by agarose gel electrophoresis.
JC-1 staining was applied to measure mitochondrial dysfunction. Caspase activation and reactive oxidative species (ROS) generation
were also measured.
Results
VK3 exhibited cytotoxicity that caused DNA fragmentation in MCF-7 cells with an IC50 of 14.2 μM. JC-1 staining revealed that VK3 caused mitochondrial dysfunction including a disappearance of mitochondrial membrane potential. Additional investigation
showed that the mitochondrial damage was induced by the generation of ROS and the subsequent activation of caspase-7 and -9.
Conclusions
Our findings demonstrate that VK3-induced apoptosis is selectively initiated by the mitochondria-related pathway and might be useful in breast cancer chemotherapy.
Keywords Vitamin K3
- Breast cancer - ROS - Mitochondrial dysfunction