Abstract
Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Moreover, additional overexpression of JNK1 led to partially antagonize the antiapoptotic environment attained by Bcl-xL, implying that JNK1-involved pathway may play a role in down-regulation of the antiapoptotic effect of Bcl-xL. However, the antagonistic effect of JNK1 on the antiapoptotic action of Bcl-xL was significantly weaker than that on the action of Bcl-2. Interestingly, we found that overexpression of JNK1 led to increase of Bcl-xL expression. Thus, these results suggest that Bcl-xL and Bcl-2 may induce its antiapoptotic effect in a different mechanism, provoking the possibility of involvement of JNK1-involved pathway in Bcl-xL expression.
Original language | English (US) |
---|---|
Pages (from-to) | 1686-1690 |
Number of pages | 5 |
Journal | Biological and Pharmaceutical Bulletin |
Volume | 31 |
Issue number | 9 |
DOIs | |
State | Published - Sep 2008 |
Externally published | Yes |
Keywords
- Antiapoptotic action
- Apoptosis
- B-cell lymphoma extra long expression
- C-jun n-terminal protein kinase signaling pathway
- Etoposide
ASJC Scopus subject areas
- Pharmacology
- Pharmaceutical Science