ArticleJournal of the Korean Society of Coloproctology2010
Effects of DCA on Cell Cycle Proteins in Colonocytes.
Article in Journal of the Korean Society of Coloproctology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- Dissecting the role of the gut microbiome and fecal microbiota transplantation in radio- and immunotherapy treatment of colorectal cancer.Frontiers in cellular and infection microbiology · 2023Review
- Implication of gut microbes and its metabolites in colorectal cancer.Journal of cancer research and clinical oncology · 2023Review
- Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A-dependent manner.Journal of cellular and molecular medicine · 2020Article
- Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer.International journal of molecular sciences · 2019Review
- Microbiota in cancer development and treatment.Journal of cancer research and clinical oncology · 2019Review
- Dysbiosis of gut microbiota in promoting the development of colorectal cancer.Gastroenterology report · 2018Review
- Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer.Digestive diseases and sciences · 2014Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEvidence 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.
methodsNormal 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.
resultsThe 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.
conclusionThe 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.
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