Effect of AZD8330 on proliferation and apoptosis of multiple myeloma cells / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 1311-1315, 2014.
Article
em Zh
| WPRIM
| ID: wpr-340507
Biblioteca responsável:
WPRO
ABSTRACT
This study was aimed to investigate the effect of MEK inhibitor AZD8330 on proliferation and apoptosis of multiple myeloma IM9 and NCI-H929 cell lines and its possible mechanism. These two cell line cells were exposed to different concentrations of AZD8330 for 48 h. The CCK-8 assay was used to detect cell viability and the IC50 value at 48 h. These above-mentioned IM9 and NCI-H929 cells were treated with 5,10 and 100 nmol/L of AZD8330, then the change of cell cycle was analysed by flow cytometry with PI staining. The Wester blot was used to detect the expression levels of cyclin D and cyclin E, and multiple myeloma cells were treated with 10, 100, 1000 and 2000 nmol/L of AZD8330, the AnnexinV/7-AAD double staining was used to analyse cell apoptosis and the Western blot was used to detect the expression level of caspase-3. The results showed that AZD8330 could significantly inhibit the cell viability of IM9 and NCI-H929 cell lines in a time-and dose-dependent manner, the IC50 value (48 h) of IM9 and NCI-H929 were 19.88 ± 2.7 nmol/L and 29.3 ± 2.03 nmol/L respectively, these two cell lines were arrested on G1 phase of cell cycle, the apoptosis cells increased along with enhancement of AZD8330 concentration, and the expression level of cleaved caspase-3 protein was up-regulated. It is concluded that AZD8330 can efficiently inhibit the proliferation of NCI-H929 and IM9 cell lines, and induce apoptosis, suggesting that the AZD8330 may be a potential chemotherapeutic candidate for multiple myeloma therapy.
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1
Índice:
WPRIM
Assunto principal:
Patologia
/
Farmacologia
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Di-Hidropiridinas
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Ciclo Celular
/
Apoptose
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Proteínas Oncogênicas
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Ciclina E
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Linhagem Celular Tumoral
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Inibidores de Proteínas Quinases
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Proliferação de Células
Limite:
Humans
Idioma:
Zh
Revista:
Journal of Experimental Hematology
Ano de publicação:
2014
Tipo de documento:
Article