Elsevier

Nutrition

Volume 17, Issues 7–8, July–August 2001, Pages 652-653
Nutrition

Research letter
Folate and chemoprevention of colorectal cancer: is 5-methyl-tetrahydrofolate an active antiproliferative agent in folate-treated colon-cancer cells?

https://doi.org/10.1016/S0899-9007(01)00594-9Get rights and content

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    While a study conducted in our laboratory showed that supplementation of supraphysiological (25 times higher) FA levels resulted in an increased number of ACF's in F344 rats (Nicken et al., 2012), an increased FA concentration in the cell culture medium did neither significantly enhance the cell transformation rate nor exert a statistically significant influence on the CFE. This might be explained, as in the case of MET, by the induction of a cell cycle arrest and other antiproliferative effects, as has been shown by Akoglu et al. (2001) in colon cancer cells receiving up to 22 μM FA. However, it should be pointed out that other studies describe a dose-dependent increase of cellular proliferation in neurosphere cultures starting at similar concentrations as used herein (18 μM; Liu et al., 2010).

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    As concentrations of purine/pyrimidine decrease, biochemical repair mechanisms may decrease the conversion of 5,10-methylenetetrahydrofolate (5,10-methyleneTHF) to 5-methyltetrahydrofolate (5-methyl THF). This is an irreversible reaction, and thereby leads to less folate availability for DNA methylation [7]. Hence, DNA methylation level can be altered by intermediary moiety 5-methyl THF, which is needed to methylate homocysteine to methionine.

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    Thus, a prediction of the model is that a high intracellular folate level can have the same effect as a folate deficiency. This prediction of the model is now supported by a variety of clinical and experimental data that show that high doses of folate can have detrimental effects (Akoglu et al., 2001; Czeizel, 2004; Morris et al., 2005; Sunder‐Plassman et al., 2000; Troen et al., 2006). We then expanded the model of Reed et al. (2006) to include compartmentation of the folate cycle between cytosol and mitochondria (Nijhout et al., 2007a).

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    Indeed, numerous studies suggested that low folate intake increased carcinogenesis [39,40]. Moreover DHF and methyl-THF had an antiproliferative effect in human colon cancer cell line in vitro [41,42]. At last, Levy and coll.

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