The accumulation of ascorbic acid by squamous cell carcinomas of the lung and larynx is associated with global methylation of DNA

Piyathilake, Chandrika J.; Bell, Walter C.; Johanning, Gary L.; Cornwell, Phillip E.; Heimburger, Douglas C.; Grizzle, William E.

doi:10.1002/1097-0142(20000701)89:1<171::aid-cncr22>3.0.co;2-o

Cited by 28 publications

(9 citation statements)

References 29 publications

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“…A deficiency of this nutrient has been associated with DNA hypomethylation in cancer cells [Piyathilake et al, 2000] However, the estimated prevalence of inadequate intakes for the New Zealand population is less than 1% [New Zealand Ministry of Health, 1999].…”

Section: Vitamin Cmentioning

confidence: 99%

Epigenetic events and protection from colon cancer in New Zealand

Ferguson

Karunasinghe

Philpott

2004

Environ and Mol Mutagen

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The incidence of colon cancer is high in many developed nations, especially New Zealand. Molecular understanding of the nature of colon cancer shows a disease whose well-characterized morphological progression is paralleled at the cellular level by increased numbers of gene or chromosome mutations, loss of heterozygosity, changed methylation patterns, and genomic instability. In the present study, we consider whether an imbalance of factors that affect DNA methylation patterns might explain at least part of the high colon cancer incidence in New Zealand. Folate is the major micronutrient whose intake impacts methylation, particularly through interaction with choline and methionine. Folate is generally somewhat deficient in the New Zealand diet, with the voluntary addition of folate to white flour not producing desired levels. Selenium affects methylation status in several ways and is recognized as being low in New Zealand soils and, therefore, diet. Zinc is also low in the diets of some New Zealand population groups, which can lead to hypomethylation. Several of the components of fruits and vegetables affect methylation patterns, and the average New Zealand intake, at two to three servings per day, is considerably below recommended amounts. Low dietary fiber, high tobacco use, and increasing rates of obesity are also likely New Zealand risk factors that may impact on methylation status. Dietary supplementation is not as common in New Zealand as in countries such as the United States, but may provide a way to raise the levels of nutrients and phytochemicals affecting methylation status, thereby enhancing colon cancer protection.

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Section: Vitamin Cmentioning

confidence: 99%

Epigenetic events and protection from colon cancer in New Zealand

Ferguson

Karunasinghe

Philpott

2004

Environ and Mol Mutagen

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“…It also has been reported that 73.9% ( n = 2668) of people in India have prevalence of vitamin C deficiency [39]. Vitamin C deficiency is associated with DNA hypermethylation in lung cancer cells [40]. In addition, Chung et al [41] have recently reported that vitamin C mediated DNA demethylation occurs most frequently at CpGs and speculated that vitamin C may indirectly change DNA topology by affecting the histone-acetylation.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Silencing of CXCR4 Promotes Loss of Cell Adhesion in Cervical Cancer

Yadav

Prasad

Das

et al. 2014

BioMed Research International

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In the network of chemokine signaling pathways, recent reports have described the SDF-1α/CXCR4 axis and its role in cancer progression and metastasis. Interestingly, we found downregulation of CXCR4 at both transcript and protein level in cervical cancer cell lines and primary tumors. We also found CXCR4 promoter hypermethylation in cervical cancer cell lines and primary biopsy samples. DNA hypomethylating drug 5-AZA-2′-deoxycytidine and histone deacetylase inhibitor Trichostatin A treatments in cell lines reactivate both CXCR4 transcription and protein expression. Cell adhesion assay demonstrated that autocrine SDF-1α promotes the loss of cell adhesion while paracrine SDF-1α predominantly protects the normal cervical cells from loss of cell adhesion. Cervical cancer cell line C-33A having increased expression of CXCR4 after TSA treatment showed increased cell adhesion by paracrine source of SDF-1α in comparison to untreated C-33A. These findings demonstrate the first evidence that epigenetic silencing of CXCR4 makes the cells inefficient to respond to the paracrine source of SDF-1α leading to loss of cell adhesion, one of the key events in metastases and progression of the disease. Our results provide novel insight of SDF-1α/CXCR4 signaling in tumor microenvironment which may be promising to further delineate molecular mechanism of cervical carcinogenesis.

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“…This may in turn cause histone hypomethylation and genomic DNA hypomethylation [13][14][15][16][17]. DNA hypermethylation in lung cancer cells can occur due to vitamin C deficiency [18,19]. Niacin, by stopping the enzymatic DNA methylation, can help to maintain the unmethylated state of CpG dinucleotides [20,21].…”

Section: Effect Of Diet and Nutrients On Dna Me-thylationmentioning

confidence: 99%

Effect Of Diet and Nutrients on Molecular Mechanism of Gene Expression Mediated By Nuclear Receptor and Epigenetic Modulation

Jalili¹

2013

TONUTRAJ

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Abstract:Major research progress in the last few decades has elucidated the complex nexus between nutrition and health. Diet and lifestyle influence epigenetic changes that are heritable. However, a statement of reservation is needed here, viz. that it is often difficult to distinguish between epigenetic changes that are inherited from one generation to the next and true mutations, for instance in mitochondrial DNA. The last topic is a big one in its own right and will not be further discussed in this article. Epigenetic changes induced by dietary nutrients ultimately culminate in changes of the expression of genes through transcription and translation. The interaction between dietary nutrients and nuclear receptors triggers the signaling pathway, leading to modulation of epigenetic change and gene expression. Knowledge about nuclear receptors is important for explaining dietary modulation of transcription via recruitment of large protein complexes. These proteins are capable of causing modification of chromosomal components, can influence chromatin proteins, and affect the binding of proteins to particular parts of the DNA molecules controlling the expression of individual genes. Chromatin complexes between DNA and proteins can be destabilized by recruitment of transcriptional coactivators by histone acetylation. However, in the presence of hormone antagonists or in the absence of relevant ligands, recruitment of other cellular core proteins may stabilize chromatin by their influence on histone deacetylases, thus antagonizing the effect of enzymes causing histone acetylation. This article reviews the current knowledge on nutritional modulation of bioactive molecules by epigenetic changes, if they can regulate genetic expressions. The molecular mechanism of action of various dietary nutrients on gene expression mediated by nuclear receptors is also discussed.

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The accumulation of ascorbic acid by squamous cell carcinomas of the lung and larynx is associated with global methylation of DNA

Cited by 28 publications

References 29 publications

Epigenetic events and protection from colon cancer in New Zealand

Epigenetic events and protection from colon cancer in New Zealand

Epigenetic Silencing of CXCR4 Promotes Loss of Cell Adhesion in Cervical Cancer

Effect Of Diet and Nutrients on Molecular Mechanism of Gene Expression Mediated By Nuclear Receptor and Epigenetic Modulation

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