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Published on: October 5, 2012

Diallyl trisulfide selectively causes Bax- and Bak-mediated apoptosis in human lung cancer cells

Dong Xiao1, Yan Zeng, Eun-Ryeong Hahm

  • 1Department of Pharmacology and Chemical Biology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.

Environmental and Molecular Mutagenesis
|September 19, 2008
PubMed

Insights

Diallyl trisulfide (DATS), a garlic compound, effectively inhibits human lung cancer cell growth by inducing cell cycle arrest and apoptosis. Bax and Bak proteins are key targets in this DATS-mediated cancer cell death process.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Garlic organosulfur compounds (OSCs) show promise in preventing chemically induced lung cancer in animal models.
  • Diallyl trisulfide (DATS) is a key OSC with potential anti-cancer properties.

Purpose of the Study:

  • To investigate the effects of DATS on human lung cancer cell viability, cell cycle, and apoptosis.
  • To compare DATS's efficacy on lung cancer cells versus normal bronchial epithelial cells.
  • To elucidate the molecular mechanisms underlying DATS-induced apoptosis.

Main Methods:

  • Cultured human lung cancer cell lines (H358, H460) and a normal bronchial epithelial cell line (BEAS-2B) were treated with DATS.
  • Cell viability, cell cycle progression, and apoptosis were assessed.
  • Protein expression levels of key cell cycle regulators (Cdk1, Cdc25C) and apoptosis-related proteins (Bax, Bak, Bcl-2, Bcl-xL, BID) were analyzed.
  • Gene silencing (siRNA) was used to investigate the role of Bax and Bak.

Main Results:

  • DATS significantly suppressed the viability of H358 and H460 lung cancer cells, inducing G2-M phase cell cycle arrest and apoptosis.
  • Normal BEAS-2B cells showed greater resistance to DATS-induced growth inhibition and apoptosis compared to cancer cells.
  • DATS induced G2-M arrest via down-regulation of Cdk1 and Cdc25C, leading to inactive Cdk1.
  • DATS-induced apoptosis involved the upregulation of Bax and Bak, and downregulation of Bcl-2 and Bcl-xL.
  • Knockdown of Bax and Bak significantly protected cells from DATS-induced apoptosis.

Conclusions:

  • DATS exhibits selective toxicity towards human lung cancer cells.
  • DATS induces apoptosis in lung cancer cells through modulation of Bcl-2 family proteins, with Bax and Bak being critical mediators.
  • DATS represents a potential therapeutic agent for lung cancer, warranting further investigation.

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