Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / drug effects
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Actins / genetics
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Actins / metabolism*
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Adenomatous Polyposis Coli Protein / genetics
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Adenomatous Polyposis Coli Protein / physiology*
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Animals
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Butyrates / pharmacology*
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Cell Division / drug effects
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Cell Movement / drug effects
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Cell Movement / genetics
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Colorectal Neoplasms / genetics
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Colorectal Neoplasms / metabolism
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Colorectal Neoplasms / prevention & control*
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Cytoskeleton / metabolism
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Cytoskeleton / physiology*
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Disease Models, Animal
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Epithelial Cells
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Flow Cytometry
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Genes, APC*
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Genes, Tumor Suppressor
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Microscopy, Fluorescence
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Mutation
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Polymerase Chain Reaction
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Sensitivity and Specificity
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Tumor Cells, Cultured
Substances
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Actins
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Adenomatous Polyposis Coli Protein
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Butyrates