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Diallyl disulfide selectively causes checkpoint kinase-1 mediated G2/M arrest in human MGC803 gastric cancer cell

Hui Ling1, Li-Feng Lu1, Jie He1

  • 1Key Laboratory of Tumor Cellular and Molecular Pathology (University of South China), College of Hunan Province, Cancer Research Institute, Hengyang, Hunan 421001, P.R. China.

Oncology Reports
|September 2, 2014
PubMed

Insights

Diallyl disulfide (DADS) from garlic halts gastric cancer cells by activating Chk1 kinase, which targets CDC25C and cyclin B1, leading to G2/M cell cycle arrest.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • Diallyl disulfide (DADS), a garlic-derived compound, exhibits anticancer properties.
  • DADS induces G2/M cell cycle arrest in human gastric cancer cells (MGC803).
  • Checkpoint kinases (Chk1 and Chk2) are crucial regulators of cell cycle arrest.

Purpose of the Study:

  • Investigate the specific roles of Chk1 and Chk2 in DADS-induced G2/M cell cycle arrest.
  • Elucidate the molecular mechanisms underlying DADS's effect on gastric cancer cell cycle progression.

Main Methods:

  • Northern blot analysis to assess mRNA expression of Chk1 and Chk2.
  • Western blot analysis to detect phosphorylated Chk1, Chk2, and ATR.
  • Immunoprecipitation assays to determine protein interactions.
  • Overexpression and knockdown studies of Chk1 and Chk2 in MGC803 cells.

Main Results:

  • DADS did not alter Chk1 or Chk2 mRNA levels.
  • DADS increased phosphorylated Chk1 and phospho-ATR, while downregulating CDC25C and cyclin B1.
  • Chk1, but not Chk2, was found to interact with CDC25C.
  • Overexpression of Chk1 enhanced DADS-induced G2/M arrest and CDC25C inhibition.
  • Chk1 knockdown abrogated DADS-induced G2/M arrest and CDC25C/cyclin B1 downregulation.

Conclusions:

  • Chk1 is the key mediator of DADS-induced G2/M cell cycle arrest in MGC803 gastric cancer cells.
  • The ATR/Chk1/CDC25C/cyclin B1 signaling pathway is essential for the DADS-mediated G2/M checkpoint response.

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