Butyrate restores motile function and actin cytoskeletal network integrity in Apc mutated mouse colon epithelial cells

被引：30

作者：

Forest, V ^{[1
]}

Clément, M ^{[1
]}

Pierre, F ^{[1
]}

Meflah, K ^{[1
]}

Menanteau, J ^{[1
]}

机构：

[1] INSERM, U419, HNRC Nantes, F-44035 Nantes 01, France

来源：

NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL | 2003年 / 45卷 / 01期

关键词：

D O I：

10.1207/S15327914NC4501_10

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Loss of function of the Apc gene product is an early and frequent event in colorectal carcinogenesis. Altered migration of intestinal epithelial cells has been described in vivo in the Min mouse Apc+/Min model. Using cell lines established from this model we show in vitro that Apc+/Min cells are less motile than Apc+/+ cells and exhibit a disordered actin cytoskeletal network This would increase the probabilities of the initiated cell to acquire additional genetic alterations leading to neoplasia. Butyrate, a product of indigestible carbohydrate fermentation by the colonic flora, is able to restore both motility and actin cytoskeletal organization. This feature may contribute to explain the protective effect exerted by butyrogenic diets on colon carcinogenesis in animal models.

引用

页码：84 / 92

页数：9

共 34 条

[21] The adenomatous polyposis coli tumor suppressor protein localizes to plasma membrane sites involved in active cell migration [J].