Transcription of the protein kinase C-delta gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin
Experimental & Molecular Medicine
;
: 699-708, 2008.
Artículo
en Inglés
| WPRIM
| ID: wpr-167143
ABSTRACT
Expression of protein kinase C-delta (PKC delta) is up-regulated by apoptosis-inducing stimuli. However, very little is known about the signaling pathways that control PKC delta gene transcription. In the present study, we demonstrate that JNK stimulates PKC delta gene expression via c-Jun and ATF2 in response to the anticancer agent doxorubicin (DXR) in mouse lymphocytic leukemia L1210 cells. Luciferase reporter assays showed that DXR-induced activation of the PKC delta promoter was enhanced by ectopic expression of JNK1, c-Jun, or ATF2, whereas it was strongly reduced by expression of dominant negative JNK1 or by treatment with the JNK inhibitor SP600125. Furthermore, point mutations in the core sequence of the c-Jun/ATF2 binding site suppressed DXR-induced activation of the PKC delta promoter. Our results suggest an additional role for a JNK signaling cascade in DXR-induced PKC delta gene expression.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Transcripción Genética
/
Transducción de Señal
/
Doxorrubicina
/
Regiones Promotoras Genéticas
/
Proteínas Proto-Oncogénicas c-jun
/
Apoptosis
/
Línea Celular Tumoral
/
Proteína Quinasa 8 Activada por Mitógenos
/
Proteína Quinasa C-delta
/
Factor de Transcripción Activador 2
Límite:
Animales
Idioma:
Inglés
Revista:
Experimental & Molecular Medicine
Año:
2008
Tipo del documento:
Artículo
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