Abstract
Carcinogenesis involves an accumulation of genetic mutations and epigenetic alterations. DNA methylation, a dynamic epigenetic modification, may underlie genomic instability, silencing of genes with tumor suppressor functions, and activation of genes associated with cancer progression. Therefore, reversing DNA methylation patterns established during carcinogenesis constitutes a promising anti-cancer strategy. Interestingly, studies have indicated that certain dietary polyphenols, such as those from catechol and stilbenoid classes present in grapes, blueberries, and green tea, exert anti-cancer effects through epigenetic regulation of gene expression. A basis of evidence demonstrating the importance of DNA methylation in cancer formation and progression as well as the impact of catechol and stilbenoid compounds on these events are presented in this review. In vitro and in vivo evidence for the chemopreventive and therapeutic potential of polyphenols through their influence on DNA methylation is discussed. Current mechanistic insights on the changes in DNA methylation machinery upon exposure to polyphenols are further emphasized. Such studies are ongoing and crucially needed for transition into application of polyphenols as agents in cancer prevention and/or treatment in the clinical setting.
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Abbreviations
- AP-1:
-
Activator protein 1
- APC:
-
Adenotamous polyposis coli
- ATM:
-
Ataxia telangiectasia mutated
- ATR:
-
Ataxia telangiectasia and rad3-related protein
- BRCA1:
-
Breast cancer 1
- CDK:
-
Cyclin-dependent kinase
- CHK1/2:
-
Checkpoint kinase 1/2
- COMT:
-
Catechol-O-methyltransferase
- DNA:
-
Deoxyribonucleic acid
- DNMT:
-
DNA methyltransferase
- EGCG:
-
Epigallocatechin gallate
- EMT:
-
Epithelial-to-mesenchymal transtion
- ER:
-
Estrogen receptor
- EXOSC4:
-
Exosome component 4
- GSTP1:
-
Glutathione S-transferase pi 1
- HCC:
-
Hepatocellular carcinoma
- HDAC:
-
Histone deacetylase
- IGF2:
-
Insulin-like growth factor 2
- MAML2:
-
Mastermind-like transcriptional coactivator 2
- MAPK:
-
Mitogen-activated protein kinase
- MBD2:
-
Methyl-CpG-binding domain 2
- MMP:
-
Matrix metalloproteinase
- MTHFR:
-
Methylenetetrahydrofolate reductase
- NENF:
-
Neuron-derived neurotrophic factor
- NF-κB:
-
Nuclear factor kappa B
- OCT1:
-
Octamer-binding transcription factor 1
- PCNA:
-
Proliferating cell nuclear antigen
- PI3K/Akt:
-
Phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B
- PTEN:
-
Phosphatase and tensin homolog
- RASAL2:
-
Ras-GTPase-activating protein 2
- RASSF-1α:
-
Ras association domain family member 1
- RNA:
-
Ribonucleic acid
- RXRα:
-
Retinoid X receptor A
- SAH:
-
S-adenosyl-L-homocysteine
- SAM:
-
S-adenosyl-L-methionine
- SENP6:
-
SUMO1/sentrin-specific peptidase 6
- STAT3:
-
Signal transducer and activator 3
- TNF:
-
Tumor necrosis factor
- TRAMP:
-
Transgenic adenocarcinoma of the mouse prostate
- TYMS:
-
Thymidylate synthase
- VEGF:
-
Vascular endothelial growth factor
- WBSCR22:
-
Williams-Beuren syndrome chromosome region 22
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Beetch, M., Stefanska, B. (2019). DNA Methylation in Anti-cancer Effects of Dietary Catechols and Stilbenoids: An Overview of Underlying Mechanisms. In: Patel, V., Preedy, V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham. https://doi.org/10.1007/978-3-319-55530-0_104
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