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Effect of arsenic trioxide on the expression of apoptosis-related genes in NB4 cells / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 1191-1195, 2007.
Artículo en Chino | WPRIM | ID: wpr-318760
ABSTRACT
The aim of this study was to investigate the gene expression profiles of acute promyelocytic leukemia (APL) cell line NB4 treated with arsenic trioxide (As2O3) by using cDNA microarray. cDNA probes were prepared through reverse transcription from mRNA of NB4 cells treated with or without arsenic trioxide. The probes were labeled with Cy3 and Cy5 fluorescence dyes individually, hybridized with cDNA microarray representing 201 different human genes, and their fluorescent intensities were scanned. The genes were screened through the analysis of the difference in the gene expression profile. The results showed that after the treatment of arsenic trioxide (2 micromol/L), 6 genes were up-regulated, and 12 genes related to apoptosis and signal transduction were down-regulated. The p21, survivin, cdc2 and Wee1Hu genes may be related to the differentiation and/or apoptosis of NB4 cells induced by As2O3. It is concluded that p21, survivin, cdc2 and Wee1Hu may play an important role in the mechanism underling arsenic trioxide-mediated NB4 cell apoptosis.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Óxidos / Patología / Farmacología / Arsenicales / Leucemia Promielocítica Aguda / Regulación Neoplásica de la Expresión Génica / Proteína Quinasa CDC2 / Apoptosis / Quinasas Ciclina-Dependientes / Ciclina B Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2007 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Óxidos / Patología / Farmacología / Arsenicales / Leucemia Promielocítica Aguda / Regulación Neoplásica de la Expresión Génica / Proteína Quinasa CDC2 / Apoptosis / Quinasas Ciclina-Dependientes / Ciclina B Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2007 Tipo del documento: Artículo