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1.
Journal of Experimental Hematology ; (6): 916-919, 2013.
Artículo en Chino | WPRIM | ID: wpr-284009

RESUMEN

This study was aimed to investigate the effects of proteasome inhibitor bortezomib on proliferation, apoptosis and the SHIP expression of K562 cells. K562 cells were treated with bortezomib of different concentrations. Cell proliferation was analyzed by MTT assay, cell apoptosis was detected by flow cytometry and SHIP mRNA expression was assayed by RT-PCR.The results showed that after being treated with 10, 20, 50 and 100 nmol/L bortezomib for 24 h, the inhibitory rates of K562 cells were (5.76 ± 1.47)%, (10.55 ± 1.59)%, (17.14 ± 2.05)% and (27.69 ± 3.57)% respectively, and were higher than that in control (1.30 ± 0.10); when K562 cells were treated with 20 nmol/L bortezomib for 24, 48 and 72 h, the inhibitory rates of cell proliferation were (10.55 ± 1.59)%, (16.33 ± 2.53)% and (19.78 ± 1.56)% respectively, there was statistic difference of cell proliferation rate between 24 h group and 48 h group (P < 0.05). After being treated with 10,20,50,100 nmol/L bortezomib for 24 h, the apoptotic rates of K562 cells were (12.7 ± 0.6)%, (26.9 ± 0.9)%, (32.6 ± 1.2)% and (72.5 ± 1.5)% respectively,and all higher than that in control (1.0 ± 0.5)% (P < 0.05). According to results of RT-PCR detection, the expression level of SHIP mRNA was obviously up-regulated after treatment with bortezomib, and showed statistical difference in comparison with control. It is concluded that bortezomib inhibits proliferation of K562 cells in time and concentration-dependent manner and induces apoptosis through up-regulation of SHIP gene.


Asunto(s)
Humanos , Antineoplásicos , Farmacología , Apoptosis , Ácidos Borónicos , Farmacología , Bortezomib , Proliferación Celular , Inositol Polifosfato 5-Fosfatasas , Células K562 , Monoéster Fosfórico Hidrolasas , Genética , Metabolismo , Inhibidores de Proteasoma , Farmacología , Pirazinas , Farmacología
2.
Journal of Southern Medical University ; (12): 647-649, 2007.
Artículo en Chino | WPRIM | ID: wpr-268057

RESUMEN

<p><b>OBJECTIVE</b>To establish a nude mouse model of malignant ascites with human ovarian carcinoma cell line OVCAR3 which highly expresses VEGF and evaluate the therapeutic of Avastin combined with cisplan.</p><p><b>METHODS</b>Forty-eight nude mice with malignant ascites resulting from intraperitoneal transplantation of human ovarian carcinoma cell line OVCAR3 were treated with intraperitoneal injection of Avastin, cisplan, their combination, and PBS, respectively, to observe the effect on ascites development, VEGF content in the ascites, peritoneal permeability, development of new vessels and number of tumor cells in the ascites.</p><p><b>RESULTS</b>Avastin obviously inhibited ascites accumulation and peritoneal capillary permeability, reduced VEGF protein level and microvascular density in the tumor tissues and the number of red cells and tumor cells in the malignant ascites, and prolonged the survival of the mice. The combination of Avastin and cisplan further enhanced the therapeutic efficacy of Avastin.</p><p><b>CONCLUSION</b>The bio-chemotherapeutic strategy with Avastin combined with cisplan can be a promising method for treatment of malignant ascites.</p>


Asunto(s)
Animales , Femenino , Humanos , Ratones , Anticuerpos Monoclonales , Anticuerpos Monoclonales Humanizados , Protocolos de Quimioterapia Combinada Antineoplásica , Usos Terapéuticos , Ascitis , Metabolismo , Bevacizumab , Línea Celular Tumoral , Cisplatino , Sinergismo Farmacológico , Ensayo de Inmunoadsorción Enzimática , Regulación Neoplásica de la Expresión Génica , Ratones Endogámicos BALB C , Ratones Desnudos , Neovascularización Patológica , Patología , Neoplasias Ováricas , Genética , Patología , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Resultado del Tratamiento , Factor A de Crecimiento Endotelial Vascular , Genética , Metabolismo , Ensayos Antitumor por Modelo de Xenoinjerto
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