Liver cancer is the most common form of
cancer in Taiwan and it usually responds to
chemotherapy. However, patients often have side effects to the chemotherapeutic drugs. Thus new agents are urgently required to treat
liver cancer.
Chrysophanol, one of the
anthraquinone derivatives, was reported to inhibit some human
cancer cell growth which may be due to the induction of apoptosis similar to other
anthraquinone derivatives though such actions have not been reported. In the present study, we reported that
chrysophanol inhibits cell growth in Hep3B
liver cancer cells based on the following observations: 1) induc cell morphological changes; 2) decreased percentage of viable cells; 3) induced S phase arrest of cell cycle progression; 4) induced DNA damage as measured by comet assay and
DAPI staining.
Chrysophanol-induced cell death however, seems to be related to necrotic processes rather than typical apoptosis.
Chrysophanol induced
reactive oxygen species and Ca(2+) production and decreased mitochondrial membrane potential (ΔΨm) and
ATP levels in Hep3B cells. No effects were observed on known
protein regulators of apoptosis such as Bax and Bcl-2.
Chrysophanol-induced cell death took place independently of
caspase-8 and -9. Based on our findings, we propose that
chrysophanol reduces cellular
ATP levels causing a drop in energy resulting in necrotic-like cell death.