Effect of diet on colonic-programmed cell death: molecular mechanism of action

被引：21

作者：

Chapkin, RS ^{[1
]}

Fan, YY

Lupton, JR

机构：

[1] Texas A&M Univ, Fac Nutr, College Stn, TX 77843 USA

[2] Texas A&M Univ, Ctr Environm & Rural Hlth, College Stn, TX 77843 USA

来源：

TOXICOLOGY LETTERS | 2000年 / 112卷

关键词：

colon cancer; butyrate; apoptosis; diet;

D O I：

10.1016/S0378-4274(99)00263-5

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Colon cancer evolves from a progressive inhibition of apoptosis and is influenced strongly by diet. Among dietary factors, butyrate (derived from fermentable fibers) may have utility as a chemopreventive agent because of its ability to promote apoptosis. Because CD95 (APO-1/Fas) transduces signals resulting in apoptosis, we tested the hypothesis that butyrate-dependent colonocyte apoptosis is mediated by this death receptor. Treatment of immortalized mouse colon cells with Fas agonistic antibody induced cell death, indicating that Pas in colonocytes is functional. Antagonism of Fas signaling using a soluble Fas:Fc chimera blocked butyrate induction of apoptosis. Therefore, Pas receptor dependent signal transduction is required for butyrate induction of apoptosis in colonic cells. (C) 2000 Published by Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：411 / 414

页数：4

共 17 条

[1] Butyrate alters activity of specific cAMP-receptor proteins in a transgenic mouse colonic cell line [J].