ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer.
Oncotarget
; 6(25): 21704-17, 2015 Aug 28.
Article
en En
| MEDLINE
| ID: mdl-26023734
ABSTRACT
In human breast cancer, estrogen receptor-α (ERα) suppresses epithelial-mesenchymal transition (EMT) and stemness, two crucial parameters for tumor metastasis; however, the underlying mechanism by which ERα regulates these two processes remains largely unknown. Bmi1, the polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog, regulates EMT transition, maintains the self-renewal capacity of stem cells, and is frequently overexpressed in human cancers. In the present study, ERα upregulated the expression of the epithelial marker, E-cadherin, in breast cancer cells through the transcriptional down-regulation of Bmi1. Furthermore, ERα overexpression suppressed the migration, invasion, and EMT of breast cancer cells. Notably, overexpression of ERα significantly decreased the CD44high/CD24low cell population and inhibited the capacity for mammosphere formation in ERα-negative breast cancer cells. In addition, overexpression of Bmi1 attenuated the ERα-mediated suppression of EMT and cell stemness. Immunohistochemistry revealed an inverse association of ERα and Bmi1 expression in human breast cancer tissue. Taken together, our findings suggest that ERα inhibits EMT and stemness through the downregulation of Bmi1.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Neoplasias de la Mama
/
Regulación Neoplásica de la Expresión Génica
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Receptor alfa de Estrógeno
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Transición Epitelial-Mesenquimal
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Complejo Represivo Polycomb 1
Límite:
Animals
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Female
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Humans
Idioma:
En
Revista:
Oncotarget
Año:
2015
Tipo del documento:
Article
País de afiliación:
China