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Induction of apoptosis and influence of HIF-1? expression on esophageal carcinoma cell ECa109 by soybean isoflavone during hypoxia / 第三军医大学学报
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-557350
Biblioteca responsável: WPRO
ABSTRACT
Objective To study the mechanisms and effect of soybean isoflavone on esophageal carcinoma cell ECa109 during the normoxia and hypoxia. Methods The environment of hypoxia was established by GasPak method. The ECa109 cells were assigned into normal control group, soybean isoflavones group, hypoxia group, and soybean isoflavones plus hypoxia group. The effect of soybean isoflavones was determined by MTT, and FCM was used for detecting the apoptosis and cell cycle of ECa109. Electron microscope was used to observe the ultrastructural changes of ECa109 induced by soybean isoflavone. Immunohistochemistry was used to detect the changes of HIF-1? and Fas. Results Soybean isoflavone could inhibit significantly the growth of ECa109 cells in a concentration-dependent manner, and arrest the cells in G_2/M phase during normoxia and hypoxia. The inhibitory effect was elevated significantly during hypoxia, and the cell apoptosis and necrosis were observed by electron microscope. The Fas expression was elevated by soybean isoflavone during the normoxia and hypoxia, and the HIF-1? expression was down-regulated during hypoxia. Conclusion Soybean isoflavone can inhibit ECa109 cells growth by delaying the progress of cell cycle, up-regulating the Fas expression. Soybean isoflavone can inhibit the expression of HIF-1? that was increased during hypoxia, which may be the mechanism that the inhibitory effect was enhanced significantly during hypoxia.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Third Military Medical University Ano de publicação: 2003 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Third Military Medical University Ano de publicação: 2003 Tipo de documento: Artigo
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