Comparative proteomic analysis of indioside D-triggered cell death in HeLa cells.

Abstract

Medicinal plants represent a rich source of cancer drug leads. Indioside D, a furostanol glycoside isolated from Solanum mammosum, was found to possess antiproliferative activity toward a panel of human cancer cell lines. Proteomic analysis of indioside D-treated HeLa cells revealed profound protein changes related to energy production and oxidative stress, suggesting that mitochondria dysfunction plays a role in indioside D-induced apoptosis. Indioside D caused a rapid dissipation of mitochondrial transmembrane potential (DeltaPsim) and the generation of reactive oxygen species (ROS), leading to the activation of caspase-dependent apoptotic cell death. The Fas death receptor pathway was also activated following indioside D treatment, and triggered the activation of caspase-8 and cleavage of Bid, which also acted through the mitochondrial apoptosis pathway. These results suggest that indioside D induced apoptosis in HeLa cells via both intrinsic and extrinsic cell death pathways.

• Authors: Chi Chun Wong, Ying Wang, Ka-Wing Cheng, Jen-Fu Chiu, Qing-Yu He, Feng Chen
• Journal: Journal of proteome research (J Proteome Res) Vol. 7 Issue 5 Pg. 2050-8 (May 2008) ISSN: 1535-3893 [Print] United States
• PMID: 18376857 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Glycosides
• Proteome
• Reactive Oxygen Species
• Receptors, Death Domain
• Steroids
• indioside D
• Caspases

Topics

• Apoptosis (drug effects)
• Caspases (metabolism)
• Cell Line, Tumor
• Enzyme Activation
• Glycosides (chemistry, pharmacology)
• HeLa Cells (drug effects)
• Humans
• Membrane Potentials (drug effects)
• Mitochondria (drug effects, metabolism)
• Molecular Structure
• Proteome (analysis, drug effects)
• Reactive Oxygen Species (metabolism)
• Receptors, Death Domain (metabolism)
• Steroids (chemistry, pharmacology)