Garlic constituent diallyl trisulfide induced apoptosis in MCF7 human breast cancer cells

Ahmed Malki1, Muhammad El-Saadani, Ahmed S Sultan

  • 1Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria, Egypt.

Cancer Biology & Therapy
|October 14, 2009
PubMed

Insights

Garlic compound diallyl trisulfide (DATS) effectively suppresses human breast cancer cell growth and induces apoptosis. DATS shows promise as a novel therapeutic strategy for breast cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Chemoprevention

Background:

  • Breast cancer is a leading cause of cancer-related deaths in women.
  • Garlic-derived organosulfur compounds (OSCs) exhibit potent antitumor effects.
  • The specific mechanisms of OSCs in cancer prevention require further investigation.

Purpose of the Study:

  • To investigate the effects of diallyl trisulfide (DATS) on human breast cancer cell lines.
  • To compare DATS efficacy on MCF-7 (cancerous) and MCF-12a (non-tumorigenic) cells.
  • To elucidate the molecular mechanisms underlying DATS-induced cell death.

Main Methods:

  • MTT assay, clonogenic survival assay, ELISA, TUNEL assay, immunofluorescence, flow cytometry.
  • Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis.
  • Assessment of cell cycle progression, apoptosis, and protein expression levels.

Main Results:

  • DATS suppressed the viability of both MCF-7 and MCF-12a cells by inducing G2/M phase arrest and apoptosis.
  • Apoptosis was more pronounced in MCF-7 cells, correlating with elevated cyclin B1 levels.
  • DATS modulated the expression of key proteins, including upregulation of FAS, cyclin D1, Bax, and p53, and downregulation of Akt and Bcl-2.

Conclusions:

  • DATS effectively inhibits breast cancer cell proliferation and induces apoptosis through specific molecular pathways.
  • DATS demonstrates differential effects on cancerous versus non-tumorigenic cells.
  • DATS represents a potential novel therapeutic agent for human breast cancer treatment.

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