Apoptosis induced by penta-acetyl geniposide in C6 glioma cells is associated with JNK activation and Fas ligand induction
- Institute of Biochemistry, Chung Shan Medical University, Taichung, Taiwan (China)
- School of Applied Chemistry, Chung Shan Medical University, Taichung, Taiwan (China)
- Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan (China)
In our previous study, penta-acetyl geniposide ((AC){sub 5}GP) is suggested to induce tumor cell apoptosis through the specific activation of PKC{delta}. However, the downstream signal pathway of PKC{delta} 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{delta} isoforms. In the present study, we investigate whether JNK is involved in (AC){sub 5}GP induced apoptosis. The result reveals that (AC){sub 5}GP 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){sub 5}GP-mediated apoptosis and related proteins expression are attenuated. Furthermore, we find that the (AC){sub 5}GP 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{delta}, since rottlerin impedes (AC){sub 5}GP-induced JNK activation. Therefore, (AC){sub 5}GP mediates cell death via activation of PKC{delta}/JNK/FasL cascade signaling.
- OSTI ID:
- 20634836
- Journal Information:
- Toxicology and Applied Pharmacology, Vol. 202, Issue 2; Other Information: DOI: 10.1016/j.taap.2004.06.016; PII: S0041-008X(04)00306-0; Copyright (c) 2004 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
- Country of Publication:
- United States
- Language:
- English
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