Apoptosis induced by penta-acetyl geniposide in C6 glioma cells is associated with JNK activation and Fas ligand induction

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• 作者：Peng ; Chiung-Huei ; Tseng ; Tsui-Hwa ; Huang ; Chien-Ning ; Hsu ; Shu-Ping ; Wang ; Chau-Jong
• 关键词：(AC)5GP ; penta-acetyl geniposide ; ECL ; enhanced chemiluminescence ; Fas L ; Fas ligand ; JNK ; c-jun N-terminal protein kinase ; PKC脙脙脙脙 ; protein kinase C脙脙脙脙 ; SDS-PAGE ; sodium dodecyl sulfate polyacrylamide gel electrophoresis ; Penta-acetyl geniposide
• 刊名：Toxicology and Applied Pharmacology
• 出版年：2005
• 期刊代码：58_0041008x
• 类别：pha
• 出版时间：January 15, 2005
• 卷：202
• 期：2
• 页码：172-179
• 文件大小：1.07 M

摘要

In our previous study, penta-acetyl geniposide ((AC)₅GP) is suggested to induce tumor cell apoptosis through the specific activation of PKC脦脦. However, the downstream signal pathway of PKC脦脦 has not yet been investigated. It was shown that JNK may play an important role in the regulation of apoptosis and could be a possible downstream signal of PKC脦脦 isoforms. In the present study, we investigate whether JNK is involved in (AC)₅GP induced apoptosis. The result reveals that (AC)₅GP induces JNK activation and c-Jun phosphorylation thus stimulating the expression of Fas-L and Fas. Using SP600125 to block JNK activation shows that (AC)₅GP-mediated apoptosis and related proteins expression are attenuated. Furthermore, we find that the (AC)₅GP induces apoptosis through the activation of JNK/Jun/Fas L/Fas/caspase 8/caspase 3, a mitochondria-independent pathway. The JNK pathway is suggested to be the downstream signal of PKC脦脦, since rottlerin impedes (AC)₅GP-induced JNK activation. Therefore, (AC)₅GP mediates cell death via activation of PKC脦脦/JNK/FasL cascade signaling.