Methyl Donor Micronutrients that Modify DNA Methylation and Cancer Outcome

Mahmoud, Abeer M.; Ali, Mohamed M.

doi:10.3390/nu11030608

Cited by 185 publications

(163 citation statements)

References 207 publications

(218 reference statements)

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“…Dietary factors are thought to have a major influence on colorectal cancer risk (3) . B vitamins (including folate, vitamin B 2 , vitamin B 6 and vitamin B 12 ) and methionine are essential for methylation reactions, nucleotide synthesis, DNA stability and DNA repair through their role in regulating one-carbon metabolism (4) . One-carbon metabolism is a series of biochemical reactions that transfer single methyl groups from one site to another.…”

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confidence: 99%

Dietary B vitamin and methionine intakes and risk for colorectal cancer: a case–control study in China

et al. 2020

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AbstractB vitamins (including folate, vitamin B2, vitamin B6 and vitamin B12) and methionine are essential for methylation reactions, nucleotide synthesis, DNA stability and DNA repair. However, epidemiological evidence among Chinese populations is limited. The objective of this study was to evaluate B vitamins and methionine in relation to colorectal cancer risk in a Chinese population. A case–control study was conducted from July 2010 to April 2019. A total of 2502 patients with colorectal cancer were recruited along with 2538 age- (5-year interval) and sex-matched controls. Dietary data were collected using a validated FFQ. Multivariable logistic regression was used to assess OR and 95 % CI. The intake of folate, vitamin B2, vitamin B6 and vitamin B12 was inversely associated with colorectal cancer risk. The multivariable OR for the highest quartile v. the lowest quartile were 0·62 (95 % CI 0·51, 0·74; Ptrend < 0·001) for folate, 0·46 (95 % CI 0·38, 0·55; Ptrend < 0·001) for vitamin B2, 0·55 (95 % CI 0·46, 0·76; Ptrend < 0·001) for vitamin B6 and 0·72 (95 % CI 0·60, 0·86; Ptrend < 0·001) for vitamin B12. No statistically significant association was found between methionine intake and colorectal cancer risk. Stratified analysis by sex showed that the inverse associations between vitamin B12 and methionine intake and colorectal cancer risk were found only among women. This study indicated that higher intake of folate, vitamin B2, vitamin B6 and vitamin B12 was associated with decreased risk of colorectal cancer in a Chinese population.

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Dietary B vitamin and methionine intakes and risk for colorectal cancer: a case–control study in China

et al. 2020

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“…The major metabolic activity involves synthesis of metabolites that can modulate the epigenome by participating in one-carbon metabolism (Mischke and Plosch, 2013). Metabolites such as folate, vitamin B12, betaine, and choline are potentially involved in the synthesis of 6-methyltetrahydrofolate, which is a methyl group donor, for the generation of S-adenosylmethionine (SAM) that participates in DNA methylation processes (Kovacheva et al, 2007;Crider et al, 2012;Kok et al, 2015;Zeisel, 2017;Mahmoud and Ali, 2019). These methyl donor nutrients are found to be regulated by specific gut microbial communities such as Lactobacillus and Bifidobacteria that are known for folate production (Strozzi and Mogna, 2008;Rossi et al, 2011).…”

Section: Dna Methylationmentioning

confidence: 99%

The Epigenetic Connection Between the Gut Microbiome in Obesity and Diabetes

et al. 2020

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Metabolic diseases are becoming an alarming health issue due to elevated incidences of these diseases over the past few decades. Various environmental factors are associated with a number of metabolic diseases and often play a crucial role in this process. Amongst the factors, diet is the most important factor that can regulate these diseases via modulation of the gut microbiome. The gut microbiome participates in multiple metabolic processes in the human body and is mainly responsible for regulation of host metabolism. The alterations in function and composition of the gut microbiota have been known to be involved in the pathogenesis of metabolic diseases via induction of epigenetic changes such as DNA methylation, histone modifications and regulation by noncoding RNAs. These induced epigenetic modifications can also be regulated by metabolites produced by the gut microbiota including short-chain fatty acids, folates, biotin and trimethylamine-N-oxide. In addition, studies have elucidated the potential role of these microbial-produced metabolites in the pathophysiology of obesity and diabetes. Hence, this review focuses on the interactions between the gut microbiome and epigenetic processes in the regulation and development of obesity and diabetes, which may have potential as a novel preventive or therapeutic approach for several metabolic and other human diseases.

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“…These genes influence several pathways in processes important for cancer transformation, including cell proliferation, angiogenesis, genome maintenance, metastasis, apoptosis, and tumor metabolism (reviewed in [80]). Studies on rodents fed with a methyl-deficient diet support the role of hypomethylation in cancer transformation (reviewed in [81]). In general, hypomethylation may play a role in cancer through targeting high-and moderate-copy DNA repeats, leading to genome instability or unique DNA sequences, which results in an increase of the expression of cancer-promoting genes [76].…”

Section: Dna Methylation In Breast Cancermentioning

confidence: 99%

Interplay between BRCA1 and GADD45A and Its Potential for Nucleotide Excision Repair in Breast Cancer Pathogenesis

Pietrasik

Zajac

Morawiec

et al. 2020

IJMS

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A fraction of breast cancer cases are associated with mutations in the BRCA1 (BRCA1 DNA repair associated, breast cancer type 1 susceptibility protein) gene, whose mutated product may disrupt the repair of DNA double-strand breaks as BRCA1 is directly involved in the homologous recombination repair of such DNA damage. However, BRCA1 can stimulate nucleotide excision repair (NER), the most versatile system of DNA repair processing a broad spectrum of substrates and playing an important role in the maintenance of genome stability. NER removes carcinogenic adducts of diol-epoxy derivatives of benzo[α]pyrene that may play a role in breast cancer pathogenesis as their accumulation is observed in breast cancer patients. NER deficiency was postulated to be intrinsic in stage I of sporadic breast cancer. BRCA1 also interacts with GADD45A (growth arrest and DNA damage-inducible protein GADD45 alpha) that may target NER machinery to actively demethylate genome sites in order to change the expression of genes that may be important in breast cancer. Therefore, the interaction between BRCA1 and GADD45 may play a role in breast cancer pathogenesis through the stimulation of NER, increasing the genomic stability, removing carcinogenic adducts, and the local active demethylation of genes important for cancer transformation.

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Methyl Donor Micronutrients that Modify DNA Methylation and Cancer Outcome

Cited by 185 publications

References 207 publications

Dietary B vitamin and methionine intakes and risk for colorectal cancer: a case–control study in China

Dietary B vitamin and methionine intakes and risk for colorectal cancer: a case–control study in China

The Epigenetic Connection Between the Gut Microbiome in Obesity and Diabetes

Interplay between BRCA1 and GADD45A and Its Potential for Nucleotide Excision Repair in Breast Cancer Pathogenesis

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