Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells
Experimental & Molecular Medicine
; : e47-2013.
Article
en En
| WPRIM
| ID: wpr-223715
Biblioteca responsable:
WPRO
ABSTRACT
Here, we report that B-cell lymphoma 2 (Bcl-2) is a novel target molecule of aspirin in breast cancer cells. Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation. These events inhibited cancer cell proliferation and subsequently enhanced MCF-7 breast cancer cell apoptosis. Bcl-2 knockdown using small interfering RNA (siRNA) delayed apoptotic cell death, which correlated with increased proliferation following aspirin exposure. In contrast, Bcl-2 overexpression enhanced the onset of aspirin-induced apoptosis, which was also associated with a significant increase in Bcl-2 phosphorylation in the nucleus. Therefore, this study may provide novel insight into the molecular mechanism of aspirin, particularly its anticancer effects in Bcl-2- and estrogen receptor-positive breast cancer cells.
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Texto completo:
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Índice:
WPRIM
Asunto principal:
Fosforilación
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Unión Proteica
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Núcleo Celular
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Aspirina
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Apoptosis
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Proteínas Proto-Oncogénicas c-bcl-2
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Proteínas de Unión a Tacrolimus
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Transporte Activo de Núcleo Celular
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Células MCF-7
Límite:
Humans
Idioma:
En
Revista:
Experimental & Molecular Medicine
Año:
2013
Tipo del documento:
Article