Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Añadir filtros








Intervalo de año
1.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 717-24, 2013.
Artículo en Inglés | WPRIM | ID: wpr-636369

RESUMEN

Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, caspase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS production was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce G1 phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 717-724, 2013.
Artículo en Inglés | WPRIM | ID: wpr-251404

RESUMEN

Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, caspase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS production was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce G1 phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.


Asunto(s)
Humanos , Antineoplásicos , Química , Farmacología , Apoptosis , Genética , Western Blotting , Neoplasias de la Mama , Genética , Metabolismo , Patología , Caspasa 8 , Genética , Metabolismo , Caspasas , Genética , Metabolismo , Proliferación Celular , Tamaño de la Célula , Ciclina D1 , Genética , Metabolismo , Quinasa 4 Dependiente de la Ciclina , Genética , Metabolismo , Citocromos c , Genética , Metabolismo , Relación Dosis-Respuesta a Droga , Fucus , Química , Puntos de Control de la Fase G1 del Ciclo Celular , Genética , Regulación Neoplásica de la Expresión Génica , Células MCF-7 , Microscopía Fluorescente , Estructura Molecular , Polisacáridos , Química , Farmacología , Proteínas Proto-Oncogénicas c-bcl-2 , Genética , Metabolismo , Especies Reactivas de Oxígeno , Metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transducción de Señal , Proteína X Asociada a bcl-2 , Genética , Metabolismo
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA