Accession Number:

ADB281645

Title:

C-Jun N-terminal Kinase and Apoptotic Signaling in Prostate Cancer

Descriptive Note:

Annual summary rept. 1 Jul 1999-31 Dec 2001

Corporate Author:

BAYLOR COLL OF MEDICINE HOUSTON TX

Personal Author(s):

Report Date:

2002-01-01

Pagination or Media Count:

37.0

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.

Subject Categories:

  • Anatomy and Physiology
  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE