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Diallyl sulfide promotes cell-cycle arrest through the p53 expression and triggers induction of apoptosis via caspase- and mitochondria-dependent signaling pathways in human cervical cancer Ca Ski cells.

Abstract
Diallyl sulfide (DAS) is a component of garlic (Alliaceae family). Although diallyl polysulfide has been shown to exhibit anticancer activities, no report explored DAS-affected cell death in human cervical cancer cells in vitro. This study investigated DAS affected on cell-cycle regulation and apoptosis in human cervical cancer Ca Ski cells. DAS at 25-100 μM decreased the viability of Ca Ski cells by increasing G0/G1 phase arrest followed by induction of apoptosis in concentration- and time-dependent effects. Flow cytomteric assay indicated that DAS (75 μM) promoted the production of Ca(2+) accumulation and decreased the level of mitochondrial membrane potential in Ca Ski cells. Western blotting showed that 75 μM of DAS-induced G0/G1 phase arrest was mediated through the increased expression of p21, p27, and p53 with a simultaneous decrease in CDK2, CDK6, and CHK2 expression. The characteristics of apoptosis, such as morphological changes and DNA condensation, altered the ratio of Bax/Bcl-2 and sub-G1 phase occurred in Ca Ski cells after exposure to DAS. Furthermore, DAS induced mitochondrial dysfunction, leading to the release of cytochrome c for causing apoptosis in Ca Ski cells. These findings suggest that DAS might be a potential chemotherapeutic agent for the treatment of cervical cancer.
AuthorsTsan-Hung Chiu, Kai-Ying Lan, Mei-Due Yang, Jen-Jyh Lin, Te-Chun Hsia, Chin-Tung Wu, Jai-Sing Yang, Fu-Shin Chueh, Jing-Gung Chung
JournalNutrition and cancer (Nutr Cancer) Vol. 65 Issue 3 Pg. 505-14 ( 2013) ISSN: 1532-7914 [Electronic] United States
PMID23530650 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Allyl Compounds
  • Reactive Oxygen Species
  • Sulfides
  • Tumor Suppressor Protein p53
  • allyl sulfide
  • Caspases
Topics
  • Allyl Compounds (pharmacology)
  • Apoptosis (drug effects)
  • Caspases (physiology)
  • Cell Cycle Checkpoints (drug effects)
  • Cell Line, Tumor
  • DNA Damage (drug effects)
  • Female
  • G1 Phase Cell Cycle Checkpoints (drug effects)
  • Gene Expression (drug effects)
  • Humans
  • Membrane Potential, Mitochondrial (drug effects)
  • Mitochondria (physiology)
  • Reactive Oxygen Species (metabolism)
  • Signal Transduction (physiology)
  • Sulfides (pharmacology)
  • Tumor Suppressor Protein p53 (genetics)
  • Uterine Cervical Neoplasms (metabolism, pathology)

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