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. JNK is involved in cellular signaling during apoptosis induced by various agents including Gammay-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. Different apoptotic stimuli induce JNK activation through distinct mechanisms. 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. In conclusion, our study reveals the importance of the JNK pathway in apoptotic signaling. These results provide important information for the studies of oncogenesis and the mechanisms of radiation and drug resistance in cancer cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2000
- Accession Number
- ADA385606
Entities
People
- Yi-rong Chen
Organizations
- Baylor College of Medicine