Cimiside E arrests cell cycle and induces cell apoptosis in gastric cancer cells

Arch Pharm Res. 2009 Oct;32(10):1385-92. doi: 10.1007/s12272-009-2007-2. Epub 2009 Nov 8.

Abstract

Cimiside E was isolated from the Cimicifuga heracleifolia Komarov extract, which has been previously demonstrated to possess apoptotic action on gastric cancer cells. The IC(50) value of cimiside E on gastric cancer cells for 24 h was 14.58 microM. The mechanism of apoptosis was further elucidated through western blot, RT-PCR, morphology, Annexin V-FITC/PI staining and cell cycle analysis. Cell cycle arrest was induced by cimiside E in S phase at a lower concentration (30 microM) and G2/M phase at higher concentrations (60 and 90 microM). Cimiside E mediated apoptosis through the induction of the caspase cascade for both the extrinsic and intrinsic pathways. These findings suggest that cimiside E may be an effective chemopreventive agent against cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Annexin A5 / metabolism
  • Antineoplastic Agents, Phytogenic / isolation & purification
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects*
  • Blotting, Western
  • Cell Cycle / drug effects*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cimicifuga / chemistry*
  • DNA Fragmentation / drug effects*
  • Fas Ligand Protein / metabolism
  • Humans
  • Reverse Transcriptase Polymerase Chain Reaction
  • Saponins / isolation & purification
  • Saponins / pharmacology*
  • Stomach Neoplasms / pathology*
  • Triterpenes / isolation & purification
  • Triterpenes / pharmacology*
  • fas Receptor / metabolism

Substances

  • Annexin A5
  • Antineoplastic Agents, Phytogenic
  • FAS protein, human
  • FASLG protein, human
  • Fas Ligand Protein
  • Saponins
  • Triterpenes
  • cimiside E
  • fas Receptor