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Regulation of human colonic cell line proliferation and phenotype by sodium butyrate

  • Gastrointestinal Oncology
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Abstract

Colonic butyrate may maintain mucosal differentiation and oppose carcinogenesis. We characterized butyrate effects on differentiation, proliferation, and matrix interactions in Caco-2 and SW620 human colonic cells. Differentiation was assessed by brush border enzyme activity and doubling time by serial cell counts. Motility across matrix proteins was quantitated by monolayer expansion and correlated with adhesiveness to matrix. Integrin subunit surface pools were measured by immunoprecipitation. Butyrate-stimulated differentiation inhibited proliferation and was significantly more potent than acetate in this regard. Butyrate also inhibited motility across collagen I, collagen IV, and laminin, as well as decreasing adhesiveness to these matrices and β1, α1, and α2 integrin subunit surface expression. Butyrate acts in cultured cells at clinically relevant concentrations to oppose classical malignant behavior, inhibiting proliferation and motility while promoting differentiation. Since butyrate is derived from fermentation of dietary fiber, such mechanisms may contribute to the apparent protective action of fiber against colon carcinogenesis.

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Funded by the Donaghue Foundation New Investigator Award #041 and American Institute for Cancer Research Grant #94A55 (MDB) and USPHS grant RO1-HL-28373 (JAM).

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Basson, M.D., Turowski, G.A., Rashid, Z. et al. Regulation of human colonic cell line proliferation and phenotype by sodium butyrate. Digest Dis Sci 41, 1986–1993 (1996). https://doi.org/10.1007/BF02093601

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  • DOI: https://doi.org/10.1007/BF02093601

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