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Updated: Jun 5, 2026
Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
Published on: April 27, 2018
ROS-Ca(2+) is associated with mitochondria permeability transition pore involved in surfactin-induced MCF-7 cells
Xiao-Hong Cao1, Si-Si Zhao, Dong-Yue Liu
1Key Laboratory of Food Nutrition and Safety (Tianjin University of Science & Technology), Ministry of Education, China.
Abstract:
The surfactin can inhibit proliferation and induce apoptosis in cancer cells. Moreover, surfactin can induce cell death in human breast cancer MCF-7 cells through mitochondrial pathway. However, the molecular mechanism involved in this pathway remains to be elucidated. Here, the reactive oxygen species (ROS) and Ca(2+) on mitochondria permeability transition pore (MPTP) activity, and MCF-7 cell apoptosis which induced by surfactin were investigated. It is found that surfactin evoked mitochondrial ROS generation, and the surfactin-induced cell death was prevented by N-acetylcysteine (NAC, an inhibitor of ROS). An increasing cytoplasmic Ca(2+) concentration was detected in surfactin-induced MCF-7 apoptosis, which was inhibited by 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM, a chelator of calcium). In addition, the relationship between ROS generation and the increase of cytoplasm Ca(2+) was determined. The results showed that surfactin initially induced the ROS formation, leading to the MPTP opening accompanied with the collapse of mitochondrial membrane potential (ΔΨ(m)). Then the cytoplasmic Ca(2+) concentration increased in virtue of the changes of mitochondrial permeability, which was prevented by BAPTA-AM. Besides, cytochrome c (cyt c) was released from mitochondria to cytoplasm through the MPTP and activated caspase-9, eventually induced apoptosis. In summary, surfactin has notable anti-tumor effect on MCF-7 cells, however, there was no obvious cytotoxicity on normal cells.
Insights
Surfactin triggers cancer cell death by inducing mitochondrial reactive oxygen species (ROS) and calcium release, leading to apoptosis in MCF-7 cells without harming normal cells.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Surfactin exhibits anti-cancer properties by inhibiting proliferation and inducing apoptosis.
- The specific mitochondrial pathway and molecular mechanisms underlying surfactin-induced apoptosis in human breast cancer MCF-7 cells require further elucidation.
Purpose of the Study:
- To investigate the roles of reactive oxygen species (ROS) and calcium (Ca2+) in surfactin-induced apoptosis.
- To elucidate the involvement of the mitochondrial permeability transition pore (MPTP) in this process.
Main Methods:
- Measurement of mitochondrial ROS generation.
- Assessment of cytoplasmic Ca2+ concentration changes.
- Analysis of mitochondrial membrane potential (ΔΨm) and MPTP activity.
- Detection of cytochrome c (cyt c) release and caspase-9 activation.
Main Results:
- Surfactin induced mitochondrial ROS generation, which was mitigated by N-acetylcysteine (NAC).
- Surfactin increased cytoplasmic Ca2+ levels, an effect inhibited by BAPTA-AM.
- Surfactin initiated ROS production, leading to MPTP opening, mitochondrial membrane potential collapse, and subsequent Ca2+ influx.
- Cytochrome c release and caspase-9 activation were observed, culminating in apoptosis.
Conclusions:
- Surfactin induces apoptosis in MCF-7 cells via a mitochondrial pathway involving ROS generation, MPTP opening, and Ca2+ dysregulation.
- The study clarifies the molecular cascade initiated by surfactin, highlighting its anti-tumor potential.
- Surfactin demonstrated selective cytotoxicity, with no significant impact on normal cells.
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