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Triptolide inhibits proliferation and induces apoptosis of imatinib resistant K562/G01 cells / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 1148-1152, 2013.
Artículo en Chino | WPRIM | ID: wpr-283964
ABSTRACT
This study was aimed to explore the inhibitory effect of triptolide on proliferation and inducing apoptosis effect of K562/G01 cells and their possible mechanism. MTT assay was used to detect the effect of imatinib or triptolide alone and their combination on K562/G01 proliferation; the cell cycle, apoptosis rate, P-gp protein expression were detected by flow cytometry (FCM); the expression of P-gp was assessed by Western blot; the BCR/ABL gene expression was assayed by real time quantitative PCR. The results showed that triptolide could enhance the effect of imatinib on proliferation inhibition and apoptosis of K562/G01, arrested the cell cycle in G1 phase, down-regulated the expression of BCR/ABL gene and P-gp protein. It is concluded that triptolide induces K562/G01 cell proliferation inhibition and apoptosis, the mechanism may be related to cell cycle arrest, decrease of P-gp protein expression, inhibition of BCR/ABL gene expression.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Fenantrenos / Piperazinas / Pirimidinas / Benzamidas / Proteínas de Fusión bcr-abl / Apoptosis / Miembro 1 de la Subfamilia B de Casetes de Unión a ATP / Resistencia a Antineoplásicos / Subfamilia B de Transportador de Casetes de Unión a ATP Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2013 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Fenantrenos / Piperazinas / Pirimidinas / Benzamidas / Proteínas de Fusión bcr-abl / Apoptosis / Miembro 1 de la Subfamilia B de Casetes de Unión a ATP / Resistencia a Antineoplásicos / Subfamilia B de Transportador de Casetes de Unión a ATP Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2013 Tipo del documento: Artículo