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Diallyl trisulfide-induced apoptosis in human cancer cells is linked to checkpoint kinase 1-mediated mitotic arrest

Dong Xiao1, Yan Zeng, Shivendra V Singh

  • 1Department of Pharmacology & Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Molecular Carcinogenesis
|May 22, 2009
PubMed

Insights

Diallyl trisulfide (DATS) causes cancer cells to arrest in mitosis via checkpoint kinase 1 (Chk1), leading to apoptosis. This process is independent of p53 status, offering new insights into cancer chemoprevention strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Diallyl trisulfide (DATS), a garlic compound, exhibits cancer chemopreventive properties.
  • DATS induces mitotic arrest in cancer cells, mediated by checkpoint kinase 1 (Chk1).
  • The ultimate fate of DATS-arrested cancer cells remains unclear.

Purpose of the Study:

  • To investigate the fate of human cancer cells undergoing DATS-induced mitotic arrest.
  • To elucidate the role of Chk1 and p53 in DATS-mediated cell cycle arrest and apoptosis.

Main Methods:

  • Utilized LNCaP and HCT-116 human cancer cell lines.
  • Analyzed cell cycle progression, apoptosis markers (caspase-3, DNA fragmentation), and protein expression (Chk1, p53, cyclins, CDKs).
  • Employed Chk1-targeted siRNA and p53 knockdown to assess their roles.

Main Results:

  • DATS induced G2/M phase arrest in both cell lines, associated with Cdk1 inactivation.
  • DATS treatment increased Chk1 phosphorylation and inactivated the anaphase-promoting complex/cyclosome.
  • Chk1 knockdown partially protected cells from DATS-induced apoptosis, while p53 knockdown did not.
  • DATS-induced mitotic arrest and subsequent apoptosis were independent of p53 status.

Conclusions:

  • DATS-induced mitotic arrest in human cancer cells is dependent on Chk1.
  • Cells arrested by DATS undergo apoptosis, irrespective of their p53 status.
  • These findings highlight DATS as a potential therapeutic agent targeting cancer cell proliferation.

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