Knockdown of the Bmi-1 oncogene inhibits cell proliferation and induces cell apoptosis and is involved in the decrease of Akt phosphorylation in the human breast carcinoma cell line MCF-7.
Oncol Rep
; 25(2): 409-18, 2011 Feb.
Article
en En
| MEDLINE
| ID: mdl-21152871
ABSTRACT
It is well documented that B cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1), widely overexpressed in the vast majority of malignancies, plays an essential role in the occurrence and development of several different tumors. Here, we report Bmi-1 siRNA-mediated cell proliferation inhibition and cell apoptosis in vitro and in vivo in the human breast carcinoma cell line MCF-7. Our results demonstrated that Bmi-1 siRNA effectively down-regulated the expression of Bmi-1, inhibited cell proliferation in vitro and in vivo, evoked cell cycle arrest in the G0/G1 phase and induced cell apoptosis in MCF-7 cells, coupled with decrease in cyclin D1, cyclin E, cdk2, bcl-2 and Ki-67 expression and Akt phosphorylation levels and an increase of p21 and bax expression and activities of caspase-3/-9. Taken together, our results suggest that Bmi-1 may be a potential molecular target for the therapy of breast carcinoma.
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Proteínas Represoras
/
Neoplasias de la Mama
/
Proteínas Nucleares
/
Carcinoma
/
Proteínas Proto-Oncogénicas
/
Apoptosis
/
ARN Interferente Pequeño
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Proliferación Celular
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Proteínas Proto-Oncogénicas c-akt
Límite:
Female
/
Humans
Idioma:
En
Revista:
Oncol Rep
Asunto de la revista:
NEOPLASIAS
Año:
2011
Tipo del documento:
Article