Jaceosidin induces apoptosis in human ovary cancer cells through mitochondrial pathway.

Abstract

We examined the antiproliferation effect of Jaceosidin (4', 5, 7-trihydroxy-3', 6-dimethoxyflavone) isolated from the herb of Artemisia vestita Wall on several human cancer cell lines. Jaceosidin significantly reduced the proliferation of CAOV-3, SKOV-3, HeLa, and PC3 cells in a concentration-dependent manner. A time-dependent inhibition was also observed in CAOV-3 cells by Jaceosidin. By flow cytometric analysis, we found that Jaceosidin treatment resulted in an increased apoptosis in CAOV-3 cells. The cells treated with Jaceosidin exhibited a decreased mitochondrial membrane potential. Jaceosidin also increased the level of cleaved caspase-9 and induced the cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP), while caspase-3 inhibitor Z-DEVD-FMK significantly reversed the proapoptotic effect of Jaceosidin in CAOV-3 cells. Moreover, Jaceosidin elevated the level of cytochrome c in cytosol. These findings suggest that the anticancer effect of Jaceosidin may be contributed by an induction of apoptosis involving cytochrome c release from mitochondria to cytosol.

• Authors: Wen Lv, Xia Sheng, Ting Chen, Qiang Xu, Xing Xie
• Journal: Journal of biomedicine & biotechnology (J Biomed Biotechnol) Vol. 2008 Pg. 394802 ( 2008) ISSN: 1110-7251 [Electronic] United States
• PMID: 18769496 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Caspase Inhibitors
• Flavonoids
• Oligopeptides
• benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone
• jaceosidin
• Cytochromes c
• Poly(ADP-ribose) Polymerases
• Caspase 3
• Caspase 9

Topics

• Apoptosis (drug effects)
• Caspase 3 (drug effects, metabolism)
• Caspase 9 (drug effects, metabolism)
• Caspase Inhibitors
• Cell Proliferation (drug effects)
• Cytochromes c (drug effects, metabolism)
• Female
• Flavonoids (pharmacology)
• HeLa Cells (drug effects)
• Humans
• Male
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (drug effects, physiology)
• Oligopeptides (pharmacology)
• Ovarian Neoplasms (metabolism)
• Poly(ADP-ribose) Polymerases (drug effects, metabolism)
• Prostatic Neoplasms (metabolism)