Emodin azide methyl anthraquinone derivative induced G0/ G1 arrest in HER2/neu-overexpressing MDA-MB-453 breast cancer cells.
J BUON
; 19(3): 650-5, 2014.
Article
em En
| MEDLINE
| ID: mdl-25261647
ABSTRACT
PURPOSE:
Our previous data have shown that emodin azide methyl anthraquinone derivative (AMAD) triggered mitochondrial- dependent cell apoptosis involving caspase-8-mediated Bid cleavage, and induced proteasomal degradation of HER2/neu by blocking Her2/neu binding to Hsp90. In the present study, we futher investigated the effect of this compound on the cell cycle and related molecular mechanisms in HER2/neu-overexpressing MDA-MB-453 breast cancer cells.METHODS:
The cell cycle distribution was tested by flow cytometry. The expression of cell cycle-related proteins was determined by Western blot analysis; DNA agarose gel electrophoresis was used to examine the apoptosis of MDAMB- 453 cells induced by emodin AMAD.RESULTS:
After MDA-MB-453 cells were treated with different concentrations of emodin AMAD for 24 hrs, cells were arrested in G0/G1 phase, and the expression of G0/G1 related proteins c/Myc, Cyclin D1, CDK4 and p-Rb changed. DNA fragmentation appeared on the agarose gel in a concentration- dependent manner.CONCLUSION:
Emodin AMAD induced G0/G1 arrest in Her2/ neu-overexpressing MDA-MB-453 cancer cells. This G0/G1 arrest was associated with decreasing protein expression of c-Myc, Cyclin D1, CDK4, and p-Rb.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Azidas
/
Antraquinonas
/
Emodina
/
Receptor ErbB-2
/
Pontos de Checagem do Ciclo Celular
/
Antineoplásicos
Limite:
Female
/
Humans
Idioma:
En
Revista:
J BUON
Assunto da revista:
NEOPLASIAS
Ano de publicação:
2014
Tipo de documento:
Article