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Diallyl disulfide causes caspase-dependent apoptosis in human cancer cells through a Bax-triggered mitochondrial

Nagathihalli S Nagaraj1, Kandangath R Anilakumar, Om V Singh

  • 1Division of Surgical Oncology, Department of Surgery, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. nagaraj.nagathihalli@vanderbilt.edu

The Journal of Nutritional Biochemistry
|May 9, 2009
PubMed

Insights

Diallyl disulfide (DADS), a garlic compound, triggers programmed cell death (apoptosis) in human cancer cells. It activates a specific mitochondrial pathway, offering potential for cancer chemoprevention and chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Diallyl disulfide (DADS), derived from garlic, shows promise as an anti-cancer agent.
  • Understanding DADS's molecular mechanisms is crucial for developing cancer therapies.

Purpose of the Study:

  • To investigate DADS-induced apoptosis in human cancer cells.
  • To elucidate the specific molecular pathways involved in DADS-mediated cell death.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analysis were used.
  • Assays for Bax translocation, cytochrome c release, and caspase activation were performed.
  • Inhibitors of caspase-3 and caspase-9 were utilized to determine the apoptotic pathway.

Main Results:

  • DADS upregulated Apaf1, cystatin B, caspase-3, and FADD expression in cancer cells.
  • DADS induced Bax translocation, cytochrome c release, and activation of caspase-3 and caspase-9.
  • Apoptosis was significantly increased in DADS-treated cells via a caspase-3-dependent pathway.

Conclusions:

  • DADS induces apoptosis in human cancer cells through a Bax-triggered, mitochondria-mediated, caspase-3-dependent pathway.
  • The mitochondrial apoptotic pathway is a key target for DADS in cancer chemoprevention and chemotherapy.

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