Effects of DCA on Cell Cycle Proteins in Colonocytes

Ha, Yun-Hyung; Park, Dong-Guk

doi:10.3393/jksc.2010.26.4.254

Cited by 11 publications

(8 citation statements)

References 17 publications

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“…Recent studies demonstrated that microbiomes had strong effects on m6A modification and expression of m6A ‘writers’ in mouse brain and intestine . By consulting the literature, we found three intestinal flora metabolites that are most closely related to the development of CRC: Short‐chain fatty acids (butyrate), DCA and ursodeoxycholic acid . In the present study, we found that butyrate, a classical intestinal microbial metabolite, could decrease the level of m6A and down‐regulate the expression of METTL3 and CCNE1 in CRC cells.…”

Section: Discussionsupporting

confidence: 56%

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Zhu

et al. 2020

J Cellular Molecular Medi

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m6A modification is the most prevalent RNA modification in eukaryotes. As the critical N6‐methyladenosine (m6A) methyltransferase, the roles of methyltransferase like 3 (METTL3) in colorectal cancer (CRC) are controversial. Here, we confirmed that METTL3, a critical m6A methyltransferase, could facilitate CRC progression in vitro and in vivo. Further, we found METTL3 promoted CRC cell proliferation by methylating the m6A site in 3′‐untranslated region (UTR) of CCNE1 mRNA to stabilize it. Moreover, we found butyrate, a classical intestinal microbial metabolite, could down‐regulate the expression of METTL3 and related cyclin E1 to inhibit CRC development. METTL3 promotes CRC proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner, representing a promising therapeutic strategy for the treatment of CRC.

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Section: Discussionsupporting

confidence: 56%

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Zhu

et al. 2020

J Cellular Molecular Medi

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“…However, colonic BAs can reach concentrations of up to 1 mM in the colon following a high-fat meal and, in humans, these are mostly secondary BAs [8,9,12]. In contrast to the effect of low secondary BA concentrations, we and others have shown that secondary Bas, such as DCA, at physiological concentrations (0.05 to 0.3 mM), inhibit colonic cell proliferation to varying degrees based on the type of cell [10,61]. Specifically, DCA and LCA promote cell cycle arrest and apoptosis primarily through the generation of intracellular reactive oxygen species (ROS), genomic DNA breakage, activation of ERK1/2, caspase-3 and poly(ADP-ribose) polymerase (PARP), but decreased cyclin E concentrations [10,60,61].…”

Section: The Impact Of Secondary Bas and Scfas On Colonic Cell Promentioning

confidence: 99%

Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer

Zeng

Umar

Rust

et al. 2019

IJMS

321

201

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Secondary bile acids (BAs) and short chain fatty acids (SCFAs), two major types of bacterial metabolites in the colon, cause opposing effects on colonic inflammation at chronically high physiological levels. Primary BAs play critical roles in cholesterol metabolism, lipid digestion, and host–microbe interaction. Although BAs are reabsorbed via enterohepatic circulation, primary BAs serve as substrates for bacterial biotransformation to secondary BAs in the colon. High-fat diets increase secondary BAs, such as deoxycholic acid (DCA) and lithocholic acid (LCA), which are risk factors for colonic inflammation and cancer. In contrast, increased dietary fiber intake is associated with anti-inflammatory and anticancer effects. These effects may be due to the increased production of the SCFAs acetate, propionate, and butyrate during dietary fiber fermentation in the colon. Elucidation of the molecular events by which secondary BAs and SCFAs regulate colonic cell proliferation and inflammation will lead to a better understanding of the anticancer potential of dietary fiber in the context of high-fat diet-related colon cancer. This article reviews the current knowledge concerning the effects of secondary BAs and SCFAs on the proliferation of colon epithelial cells, inflammation, cancer, and the associated microbiome.

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“…Histone deacetylase (HDAC) inhibitor. Binds GPR109A regulates gene expression, inflammation and autophagy Bifidobacterium Decreased in levels; having the anti-tumor activities Deoxycholic acid Activating β-catenin and epidermal growth factor receptor (EGFR) signaling [ 132 ] Clostridium Increased in levels; acting through FXR, PXR, VDR Lithocholic acid Promoting cancer invasion and MAPK signaling [ 136 ] Bacteroides fragilis Increased in levels Ursodeoxycholic acid Inhibiting the activation of COX-2 [ 146 ], blocking Ras activation [ 147 ] Decreased in levels Bacterial toxin (Fragilysin) Activating the β-catenin nuclear signaling [ 157 ] Bacteroides fragilis Increased in levels Trimethylamine-N-oxide (TMAO) Use L-carnitine or choline to produce TMAO [ 18 ] Clostridium Increased in levels …”

Section: Metabolic Role Of Gut Microbiotamentioning

confidence: 99%

“…DCA, one metabolite of the gut microbiota, has been known as a significant contributor to the development of CRC. There is evidence indicating that DCA could modulate intracellular signaling and gene expression [ 132 ]. DCA can induce cancer stemness by regulating the muscarinic 3 receptor/Wnt signaling pathway [ 133 ].…”

Section: Metabolic Role Of Gut Microbiotamentioning

confidence: 99%

Dysbiosis of gut microbiota in promoting the development of colorectal cancer

Zou

Fang

Lee

2017

Gastroenterology Report

207

182

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Gastrointestinal microbiome, containing at least 100 trillion bacteria, resides in the mucosal surface of human intestine. Recent studies show that perturbations in the microbiota may influence physiology and link to a number of diseases, including colon tumorigenesis. Colorectal cancer (CRC), the third most common cancer, is the disease resulting from multi-genes and multi-factors, but the mechanistic details between gut microenvironment and CRC remain poorly characterized. Thanks to new technologies such as metagenome sequencing, progress in large-scale analysis of the genetic and metabolic profile of gut microbial has been possible, which has facilitated studies about microbiota composition, taxonomic alterations and host interactions. Different bacterial species and their metabolites play critical roles in the development of CRC. Also, microbiota is important in the inflammatory response and immune processes deregulation during the development and progression of CRC. This review summarizes current studies regarding the association between gastrointestinal microbiota and the development of CRC, which provides insights into the therapeutic strategy of CRC.

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Effects of DCA on Cell Cycle Proteins in Colonocytes

Cited by 11 publications

References 17 publications

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer

Dysbiosis of gut microbiota in promoting the development of colorectal cancer

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