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Antitumor activity of histone deacetylase inhibitor suberic bishydroxamate on acute myeloid leukemia cell lines / 浙江大学学报·医学版
Article en Zh | WPRIM | ID: wpr-336762
Biblioteca responsable: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of histone deacetylase inhibitor suberic bishydroxamate (SBHA) on human acute myeloid leukemia (AML) cell lines.</p><p><b>METHODS</b>AML U937, KG-1 and Kasumi-1 cells were treated with SBHA. Cell growth was measured by MTT assay. Apoptosis was determined using flow cytometry. Activation of Caspase pathway and expression of apoptosis regulator proteins were detected by Western blot.</p><p><b>RESULTS</b>SBHA significantly induced growth arrest and apoptosis in U937, KG-1 and Kasumi-1 cells. Enhanced apoptosis was observed in SHBA group evidenced by strong activation of Caspase-9, Caspase-8 and Caspase-3. SHBA treatment resulted in down-regulation of anti-apoptotic protein Bcl-2 and Bcl-xl expression; down-regulated expression of antiapoptotic proteins survivin, XIAP and cIAP was also detected after SBHA treatment.</p><p><b>CONCLUSION</b>SBHA can effectively kill AML cells by inhibiting cell growth and inducing apoptosis, which is associated with the activation of Caspase pathway and regulation of apoptotic related proteins.</p>
Asunto(s)
Texto completo: 1 Índice: WPRIM Asunto principal: Patología / Farmacología / Leucemia Mieloide Aguda / Apoptosis / Caspasas / Línea Celular Tumoral / Proteínas Reguladoras de la Apoptosis / Inhibidores de Histona Desacetilasas / Ácidos Hidroxámicos / Metabolismo Límite: Humans Idioma: Zh Revista: Journal of Zhejiang University. Medical sciences Año: 2012 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Asunto principal: Patología / Farmacología / Leucemia Mieloide Aguda / Apoptosis / Caspasas / Línea Celular Tumoral / Proteínas Reguladoras de la Apoptosis / Inhibidores de Histona Desacetilasas / Ácidos Hidroxámicos / Metabolismo Límite: Humans Idioma: Zh Revista: Journal of Zhejiang University. Medical sciences Año: 2012 Tipo del documento: Article