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Apoptosis induced by diallyl disulfide in human breast cancer cell line MCF-7. | LitMetric

Apoptosis induced by diallyl disulfide in human breast cancer cell line MCF-7.

Acta Pharmacol Sin

Institute of Pharmacy and Pharmacology, College of Science and Technology, University of South China, Hengyang 421001, China.

Published: October 2008

AI Article Synopsis

  • * Experiments showed that DADS decreased MCF-7 cell growth and significantly increased the rate of apoptosis, affecting specific protein pathways involved in cell death.
  • * The findings suggest that DADS may prevent MCF-7 cell growth by inhibiting the ERK pathway and activating stress-activated pathways like SAPK/JNK and p38.

Article Abstract

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.

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Source
http://dx.doi.org/10.1111/j.1745-7254.2008.00851.xDOI Listing

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