Caspase-3-dependent protein kinase C delta activity is required for the progression of Ginsenoside-Rh2-induced apoptosis in SK-HEP-1 cells

Cancer Lett. 2005 Dec 18;230(2):228-38. doi: 10.1016/j.canlet.2004.12.043.

Abstract

Ginsenoside-Rh2 (G-Rh2) has been shown to induce apoptosis in a variety of cell types. In this study, we show that G-Rh2-induced apoptosis is accompanied by the mitochondrial release of cytochrome c and activation of caspase-3 in the human hepatoma cell line, SK-HEP-1. Furthermore, protein kinase C delta (PKCdelta) activity was markedly up-regulated in a lipid activator-independent manner with kinetics similar to those of PKCdelta and PARP cleavages during the apoptotic progression. Pre-treatment of cells with the caspase-3 specific inhibitor (z-DEVD-fmk) effectively prevented the G-Rh2-induced proteolytic activation of PKCdelta. Moreover, rottlerin, a specific PKCdelta inhibitor blocked G-Rh2-induced proapoptotic effects on the cells including the release of cytochrome c, activation of caspase-3 activity, and proteolytic cleavage and activation of PKCdelta. These results suggest that G-Rh2-induced apoptosis is functionally linked to mitochondrial dysfunction and caspase-3 activity is regulated by positive feedback with PKCdelta via the mitochondrial pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetophenones / pharmacology
  • Apoptosis*
  • Benzopyrans / pharmacology
  • Caspase 3
  • Caspases / metabolism*
  • Cell Line, Tumor
  • Cytochromes c / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Ginsenosides / pharmacology*
  • Humans
  • Protein Kinase C-delta / antagonists & inhibitors
  • Protein Kinase C-delta / metabolism*

Substances

  • Acetophenones
  • Benzopyrans
  • Enzyme Inhibitors
  • Ginsenosides
  • ginsenoside Rh2
  • Cytochromes c
  • rottlerin
  • Protein Kinase C-delta
  • CASP3 protein, human
  • Caspase 3
  • Caspases