Butyrate stimulates cyclin D and p21 and inhibits cyclin-dependent kinase 2 expression in HT-29 colonic epithelial cells.

doi:10.1006/BBRC.1997.6255

Paper

Butyrate stimulates cyclin D and p21 and inhibits cyclin-dependent kinase 2 expression in HT-29 colonic epithelial cells.

Published Mar 6, 1997 · S. Siavoshian, H. Blottière, C. Cherbut

Biochemical and biophysical research communications

Q1 SJR score

101

Citations

6

Influential Citations

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Abstract

Sodium butyrate, a product of colonic fermentation of dietary fiber, has been shown to inhibit cell proliferation by blocking the cells in the G1 phase of the cell cycle. However, its mechanism of action is still unknown. We found that butyrate strongly stimulated cyclin D and p21/WAF1/CIP1 expression in HT-29 human colonic adenocarcinoma cells, in a dose dependent manner. These stimulations were associated with a decrease in cyclin-dependent kinase (cdk) 2 level, whereas cdk4 and cdk6 remained unchanged. Our results suggest that the inhibition of cell cycle progression by sodium butyrate may be explained by a modulation of cell cycle regulatory proteins such as cyclin D and p21.

In Vitro Study

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Study Snapshot

Sodium butyrate inhibits cell proliferation by modulating cell cycle regulatory proteins like cyclin D and p21, suggesting its potential role in colonic cancer treatment.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Butyrate stimulates cyclin D and p21 and inhibits cyclin-dependent kinase 2 expression in HT-29 colonic epithelial cells.

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References

Citations

Sodium Butyrate (NaB) and Sodium Propionate (NaP) Reduce Cyclin A2 Expression, Inducing Cell Cycle Arrest and Proliferation Inhibition of Different Breast Cancer Subtypes, Leading to Apoptosis

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Antioxidant Role of Probiotics in Inflammation-Induced Colorectal Cancer

Probiotics may help prevent or delay colorectal cancer by modulating oxidative stress and inflammation-related pathways.

A Narrative Review: Immunometabolic Interactions of Host–Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers

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Epigenetic effects of short-chain fatty acids from the large intestine on host cells

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The Modulatory Effects of Fatty Acids on Cancer Progression

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