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Ha YH, Park DG. Effects of DCA on Cell Cycle Proteins in Colonocytes. J Korean Soc Coloproctol. 2010;26(4):254-9doi: 10.3393/jksc.2010.26.4.254.
Ha, Y. H., & Park, D. G. (2010). Effects of DCA on Cell Cycle Proteins in Colonocytes. Journal of the Korean Society of Coloproctology, 26(4), 254-9. https://doi.org/10.3393/jksc.2010.26.4.254
Ha, Yun-Hyung, and Park, Dong-Guk. "Effects of DCA on Cell Cycle Proteins in Colonocytes." Journal of the Korean Society of Coloproctology vol. 26,4 (2010): 254-9. doi: https://doi.org/10.3393/jksc.2010.26.4.254
Ha YH, Park DG. Effects of DCA on Cell Cycle Proteins in Colonocytes. J Korean Soc Coloproctol. 2010 Aug;26(4):254-9. doi: 10.3393/jksc.2010.26.4.254. Epub 2010 Aug 31. PMID: 21152226; PMCID: PMC2998009.
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J Korean Soc Coloproctol. 2010 Aug;26(4):254-9. doi: 10.3393/jksc.2010.26.4.254. Epub 2010 Aug 31.

Effects of DCA on Cell Cycle Proteins in Colonocytes.

Journal of the Korean Society of Coloproctology

Yun-Hyung Ha, Dong-Guk Park

Affiliations

  1. Department of Surgery, Dankook University School of Medicine, Cheonan, Korea.

PMID: 21152226 PMCID: PMC2998009 DOI: 10.3393/jksc.2010.26.4.254

Abstract

PURPOSE: Evidence that indicates bile acid is a promoter of colon cancer exists. Deoxycholic acid (DCA) modifies apoptosis or proliferation by affecting intracellular signaling and gene expression. However, because previous studies have been based on studies on colon cancer cell lines, the effect of DCA on normal colonocytes is unknown.

METHODS: Normal colonocytes and Caco-2 and HCT116 cells were treated with 20 µM and 250 µM of DCA, and the effect of different concentrations of DCA was measured based on the expression of cell-cycle-related proteins by using Western blots.

RESULTS: The expressions of CDK2 and cyclin D1 for different concentrations of DCA in normal colonocytes and colon cancer cells were similar, but the expressions of cyclin E and A were significantly different. In HCT116 colon cancer cells, the expression of cyclin E increased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin E was not changed or decreased. In HCT116 colon cancer cells, the expression of cyclin A was not changed or decreased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin A was increased at a DCA concentration of 20 µM.

CONCLUSION: The effect of DCA on stimulating cell proliferation suggests that DNA synthesis is stimulated by an increased expression of cyclin E in colon cancer cells. Our results suggest that a low dose of DCA induces cellular proliferation through increased expression of cyclin A and that a high dose of DCA induces decreased expression of cyclin E and CDK2 in normal colonocytes.

Keywords: CDK2; Cell cycle; Colonocyte; Cyclin; Deoxycholic acid

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