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Published on: January 26, 2019
Apoptosis induced by diallyl disulfide in human breast cancer cell line MCF-7
Xiao-yong Lei1, Shu-qiong Yao, Xu-yu Zu
1Institute of Pharmacy and Pharmacology, College of Science and Technology, University of South China, Hengyang 421001, China. lei_xiaoyong@yahoo.com.cn
Aim:
To investigate the effect of diallyl disulfide (DADS), a component of garlic, on apoptosis in human mammary cancer cell line (MCF-7) and its mechanisms.
Methods:
Cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assays. Morphology of apoptotic cells was detected by acridine orange and ethidium bromide staining. Apoptotic cells stained with propidium iodide were examined using flow cytometry. Protein levels were detected by Western blot analysis.
Results:
DADS inhibited the proliferation of MCF-7 cells and induced the apoptotic ratio to increase rapidly. Cleavage of the caspase-3 and caspase-3 substrate poly(ADP-ribose) polymerase was observed in MCF-7 cells after 24 h of treatment with DADS. When the MCF-7 cells were treated with 200 micromol x L DADS, the stress-activated protein kinase extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase, was inhibited after 6 h; c-Jun N-terminal kinase (JNK), that is stress-activated protein kinase (SAPK), and p38 mitogen-activated protein kinase were activated after 6 h.
Conclusion:
These results suggest that DADS both inhibits the proliferation of MCF-7 cells and induces apoptosis of MCF-7 cells. The mechanisms may include the inhibition of ERK and the activation of the SAPK/JNK and p38 pathways.
Insights
Diallyl disulfide (DADS), a garlic compound, inhibits human breast cancer cell (MCF-7) proliferation and induces apoptosis. This occurs through the inhibition of ERK and activation of SAPK/JNK and p38 pathways.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Garlic contains diallyl disulfide (DADS), a compound with potential anti-cancer properties.
- Human mammary cancer cell line (MCF-7) is a widely used model for breast cancer research.
Purpose of the Study:
- To investigate the effect of DADS on apoptosis in MCF-7 cells.
- To elucidate the underlying mechanisms of DADS-induced apoptosis.
Main Methods:
- Cytotoxicity assessed using MTT assays.
- Apoptosis detection via acridine orange/ethidium bromide staining and flow cytometry.
- Protein analysis performed using Western blot.
Main Results:
- DADS significantly inhibited MCF-7 cell proliferation.
- DADS treatment led to increased apoptosis, evidenced by caspase-3 and PARP cleavage.
- DADS modulated mitogen-activated protein kinase pathways, inhibiting ERK and activating SAPK/JNK and p38.
Conclusions:
- DADS exhibits anti-proliferative and pro-apoptotic effects on MCF-7 cells.
- The mechanisms involve the modulation of ERK, SAPK/JNK, and p38 signaling pathways.
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