C-Jun N-terminal Kinase and Apoptotic Signaling in Prostate Cancer
Abstract
Understanding the biochemical mechanisms of apoptosis is important for revealing cancer biology and for improving cancer therapies. The c-Jun N-terminal kinase (JNK) pathway participates in cellular responses to both environmental stresses and mitogenic signals. The involvement of JNK in both mitogenic and apoptotic signaling implies that a subtle regulatory mechanism must exist for the signaling decision. Our studies reveal that the duration of JNK induction may determine cell fate. JNK is involved in cellular signaling during apoptosis induced by various agents including gamma-radiation, UV-radiation, anti-carcinogenic isothiocyanates, and retinoid analog N-(4-hydroxyphenyl) retinamide (4-HPR) in various cancer cells. Interfering with the JNK pathway suppressed the induction of apoptosis. JNK activation by apoptotic stimuli can be caspase-dependent or independent. Oxidative stress induces JNK activation through the down-regulation of JNK-inactivating phosphatases. In conclusion, our study reveals the importance of the JNK pathway in apoptotic signaling. The results of this study provide important information for the studies of oncogenesis and may facilitate the development of strategies for the prevention and treatment of prostate and other cancers.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2002
- Accession Number
- ADB281645
Entities
People
- Yi-rong Chen
Organizations
- Baylor College of Medicine