Differential regulation of the antiapoptotic action of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma extra long (Bcl-xL) by c-Jun N-terminal protein kinase (JNK) 1-involved pathway in neuroglioma cells.
Biol Pharm Bull
; 31(9): 1686-90, 2008 Sep.
Article
em En
| MEDLINE
| ID: mdl-18758060
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.
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias Encefálicas
/
Proteínas Proto-Oncogênicas c-bcl-2
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Proteína Quinase 8 Ativada por Mitógeno
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Proteínas Reguladoras de Apoptose
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Proteína bcl-X
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Glioma
Idioma:
En
Ano de publicação:
2008
Tipo de documento:
Article