Annals of Coloproctology

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Effects of DCA on Cell Cycle Proteins in Colonocytes: Yun-Hyung Ha, Dong-Guk Park; J Korean Soc Coloproctol. 2010;26(4):254-259. Published online August 31, 2010; DOI: https://doi.org/10.3393/jksc.2010.26.4.254

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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.

Citations

Citations to this article as recorded by

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Deoxycholic acid inhibits the growth of BGC-823 gastric carcinoma cells via a p53-mediated pathway
HAI-BO YANG, WEI SONG, MEI-DIE CHENG, HAI-FANG FAN, XU GU, YING QIAO, XIN LU, RUI-HE YU, LAN-YING CHEN
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Sara M. Centuori, Jesse D. Martinez
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The Expression and Correlation of Cyclin E, P21WAF1Protein and P53 Variant Protein in Colorectal Adenoma and Carcinoma.: Kim, Jong Woo , Ahn, Hee Jung , Choi, Sung Woo , Ahn, Dae Ho , Chung, Jae Sam , Lee, Kyung Po; J Korean Soc Coloproctol. 1998;14(1):51-58.

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Abstract PDF: Cyclins are proteins that activate different cyclin-dependent kinases(CDKs) and promote the cell cycles. Their correlations with several human cancers have been identified. Cyclin E, as one of G1 cylins, produces DNA replication through the progression of cell cycle G1 --> S phase. In contrast, cyclin-dependent kinase inhibitors(CDKI) bound with cyclin E-cdk2 complex control the cell cycle and inhibit the cell proliferation. P21(WAF1) proteins, which are CDKIs, are transcripted by a p53 gene and participate in the cell cycle inhibition. Variant p53 proteins produced by a mutated p53 gene lose the ability to control of the cell cycle resulting in cell proliferation. This study is aimed to reveal the expressions of cyclin E, p21(WAF1) protein, p53 variant protein in colorectal adenomas and carcinomas, and also reveal their correlations in the process of carcinogenesis. Twenty-one colorectal adenomas or adenomatous polyps, and thirty colorectal carcinoma tissues were obtained by operative resections or endoscopic polypectomies. Immuno histochemical stains of the above-mentioned three proteins and a statistical analysis of their correlations were made. The results were as follows: 1. P21 proteins were expressed in the upper-one third layer of all normal colonic mucosa, but cyclin E and variant p53 protein were not identified. 2. Cyclin E was expressed in 23.8% of adenomas and 76.7% of carcinomas. Variant p53 protein was expressed in 71.4% of adenomas and 83.3% in carcinomas. The degree of positivity of variant p53 expression was correlated with cancer staging. P21 protein was expressed in all adenomas, similar to normal mucosa, but was not expressed in 43.3% of carcinomas. 3. Expression of cyclin E was increased as to the positivity of variant p53 proteins but the correlations of p21 proteins and cyclin E, and p21 proteins and variant p53 proteins were not identified. Cancer staging was not correlated with the expressions of the three proteins. In conclusion, it can be thought that the overexpression of cyclin E and variant p53 proteins, and the loss of p21 proteins are related with the colorectal carcinogenesis. We can also identify the relationship of cyclin E and variant p53 proteins.

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