Abstract
Gallbladder carcinoma is known to be an aggressive malignancy and non-sensitive to routine chemotherapy; its prognosis is quite poor. In this study, we show that emodin (1,3,8-trihydroxy-6-methylanthraquinone), an active component from Chinese medicinal herbs, can enhance apoptosis of gallbladder cancer cells induced by cisplatin (CDDP) in a reactive oxygen species (ROS)-dependent manner. The expression of survivin, which is involved in the inhibition of apoptosis, was measured after drug treatment and it was found that this could be suppressed by CDDP. Co-treatment with emodin additively inhibited survivin expression in a ROS-dependent manner. Further experiments proved that emodin potentiated the antitumor effects of CDDP in vivo by downregulating the expression of survivin without causing detectable toxic effects on normal tissues.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Antineoplastic Combined Chemotherapy Protocols / pharmacology*
-
Apoptosis / drug effects
-
Cell Growth Processes / drug effects
-
Cell Line, Tumor
-
Cell Survival / drug effects
-
Cisplatin / administration & dosage
-
Cisplatin / pharmacology*
-
Down-Regulation / drug effects
-
Drug Synergism
-
Emodin / administration & dosage
-
Emodin / pharmacology*
-
Gallbladder Neoplasms / drug therapy*
-
Gallbladder Neoplasms / metabolism
-
Gallbladder Neoplasms / pathology
-
Humans
-
Inhibitor of Apoptosis Proteins / antagonists & inhibitors*
-
Inhibitor of Apoptosis Proteins / biosynthesis
-
Mice
-
Mice, Inbred BALB C
-
Mice, Nude
-
Reactive Oxygen Species / metabolism*
-
Survivin
-
Xenograft Model Antitumor Assays
Substances
-
BIRC5 protein, human
-
Inhibitor of Apoptosis Proteins
-
Reactive Oxygen Species
-
Survivin
-
Emodin
-
Cisplatin