14-3-3σ mediates G2-M arrest produced by 5-aza-2'-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells.
Gynecol Oncol
; 127(1): 231-40, 2012 Oct.
Article
en En
| MEDLINE
| ID: mdl-22772061
ABSTRACT
OBJECTIVES:
To determine the effect of 5-aza-2'-deoxycytidine (DAC) on human endometrial carcinoma cell (HECC) oncogenicity and demonstrate a molecular mechanism by which DAC modulates HECC oncogenicity.METHODS:
The effect of DAC was tested on HECC RL95-2, AN3, Ishikawa and ECC1 cells. The role of 14-3-3σ on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3σ gene expression.RESULTS:
Treatment of HECC with DAC produced non-cytotoxic cell growth inhibition and G2/M cell cycle arrest. This effect was strongly correlated with increased expression of p21 and 14-3-3σ. Silencing of 14-3-3σ induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3σ showed the opposite effect. Furthermore, forced expression of 14-3-3σ in human endometrial cell lines reduced cell growth and colony formation.CONCLUSIONS:
We suggest that 14-3-3σ in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC.
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Base de datos:
MEDLINE
Asunto principal:
Azacitidina
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Biomarcadores de Tumor
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Neoplasias Endometriales
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Proteínas 14-3-3
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Exonucleasas
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Puntos de Control de la Fase G2 del Ciclo Celular
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Puntos de Control de la Fase M del Ciclo Celular
Idioma:
En
Revista:
Gynecol Oncol
Año:
2012
Tipo del documento:
Article