Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 143-150 |
| Number of pages | 8 |
| Journal | Cancer Chemotherapy and Pharmacology |
| Volume | 65 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2009 |
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Keywords
- Breast cancer
- Mitochondrial dysfunction
- ROS
- Vitamin K
ASJC Scopus subject areas
- Cancer Research
- Oncology
- Pharmacology
- Pharmacology (medical)
- Toxicology
Cite this
The potential of vitamin K3 as an anticancer agent against breast cancer that acts via the mitochondria-related apoptotic pathway. / Akiyoshi, Takeshi; Matzno, Sumio; Sakai, Mika; Okamura, Noboru; Matsuyama, Kenji.
In: Cancer Chemotherapy and Pharmacology, Vol. 65, No. 1, 2009, p. 143-150.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The potential of vitamin K3 as an anticancer agent against breast cancer that acts via the mitochondria-related apoptotic pathway
AU - Akiyoshi, Takeshi
AU - Matzno, Sumio
AU - Sakai, Mika
AU - Okamura, Noboru
AU - Matsuyama, Kenji
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Breast cancer
KW - Mitochondrial dysfunction
KW - ROS
KW - Vitamin K
UR - http://www.scopus.com/inward/record.url?scp=70349617472&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70349617472&partnerID=8YFLogxK
U2 - 10.1007/s00280-009-1016-7
DO - 10.1007/s00280-009-1016-7
M3 - Article
VL - 65
SP - 143
EP - 150
JO - Cancer Chemotherapy and Pharmacology
JF - Cancer Chemotherapy and Pharmacology
SN - 0344-5704
IS - 1
ER -