C-Jun N-terminal Kinase and Apoptosis in Breast Cancer.
Abstract
Previously, our laboratory demonstrated that c-Jun N-terminal kinase participates in apoptosis signaling. JNK induction is differentially regulated by mitogenic and apoptotic stimuli in T cells, and the duration of JNK activation may determine cell fate in T cells. Here, we show that JNK is also differentially regulated by mitogenic and apoptotic stimuli in breast cancer cell line MCF-7, suggesting that duration of JNK activation may also determine cell fate in breast cancer cells. Tumor suppressor p53 is not required for radiation induced JNK activation. It is also not required for apoptosis induced by JNK activation. However, our data does not exclude the possibility that p53 may mediate JNK-induced apoptosis, which needs to be further studied. Both JNK activity and Fas expression can be induced by gamma radiation; however, Fas expression is closely associated with a wild-type p53 status but not with the JNK activation. These results suggest that Fas is not the downstream target for the JNK pathway. We demonstrate that JNK is activated through oxidative stresses caused by apoptotic stimulation, since JNK activation is blocked by antioxidants, N-acetyl- cysteine and 2-mercaptoethanol. Bcl-2 suppresses JNK activation, suggesting that Bcl-2 is located in the upstream of the JNK pathway.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 1998
- Accession Number
- ADA353790
Entities
People
- Yi-rong Chen
Organizations
- Baylor College of Medicine