Nutrients and the Pancreas: An Epigenetic Perspective

Weisbeck, Andee; Jansen, Rick

doi:10.3390/nu9030283

Cited by 30 publications

(22 citation statements)

References 89 publications

(175 reference statements)

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“…Low folate intake has been associated with hypomethylation and an increased risk of colorectal and pancreatic cancers [ 9 , 34 ]. There is a growing body of epidemiological evidence that folate modulates anticarcinogenic properties through epigenetic changes, as folate deficiency reduces the potential for DNA methylation, and abnormal DNA methylation is associated with many types of cancer.…”

Section: Nutritional Epigeneticsmentioning

confidence: 99%

“…A variety of dietary factors are potential HDAC and HAT modulators. Some, such as sulforaphane, an isothiocyanate found in broccoli sprouts, or diallyl disulfide, an organosulfur compound in garlic, have been shown to act as HDAC inhibitors [ 9 , 35 ], a class of epigenetic therapeutic described further below. Such epigenetic drugs have been used to treat cancers in clinical trials due to their mode of action in restoring cancer cell differentiation and rendering tumors more sensitive to conventional therapies [ 36 ].…”

Section: Nutritional Epigeneticsmentioning

confidence: 99%

“…Many lncRNAs complex with chromatin-modifying proteins to recruit their catalytic activity to specific genomic sites, thereby modifying chromatin states and influencing gene expression. With little or no protein-coding potential, lncRNAs instead participate in various intracellular processes [ 7 ], and recent studies have identified that certain lncRNAs are specifically associated with certain cancers [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

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The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease

Tiffon

2018

IJMS

356

180

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Environmental epigenetics describes how environmental factors affect cellular epigenetics and, hence, human health. Epigenetic marks alter the spatial conformation of chromatin to regulate gene expression. Environmental factors with epigenetic effects include behaviors, nutrition, and chemicals and industrial pollutants. Epigenetic mechanisms are also implicated during development in utero and at the cellular level, so environmental exposures may harm the fetus by impairing the epigenome of the developing organism to modify disease risk later in life. By contrast, bioactive food components may trigger protective epigenetic modifications throughout life, with early life nutrition being particularly important. Beyond their genetics, the overall health status of an individual may be regarded as an integration of many environmental signals starting at gestation and acting through epigenetic modifications. This review explores how the environment affects the epigenome in health and disease, with a particular focus on cancer. Understanding the molecular effects of behavior, nutrients, and pollutants might be relevant for developing preventative strategies and personalized heath programs. Furthermore, by restoring cellular differentiation, epigenetic drugs could represent a potential strategy for the treatment of many diseases including cancer.

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Section: Nutritional Epigeneticsmentioning

confidence: 99%

Section: Nutritional Epigeneticsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease

Tiffon

2018

IJMS

356

180

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“…It was established that the risk of lung cancer decreased by 3% with every 2 mg/day increase in dietary vitamin E. In the case of pancreatic cancer, the consumption of vegetables, fruits, and whole grains has been associated with a reduced risk of disease [38]. The combination of whole grains and folate has been indicated to provide further protection against pancreatic cancer, while it was suggested to replace meat cooked at high temperatures with fish or poultry due to the negative effects exerted by the former [38,39]. Although moderate alcohol consumption has been associated with a decreased risk of pancreatic cancer, heavy drinking has been reported to enhance the risk [40].…”

Section: Nutrition and Cancer Riskmentioning

confidence: 99%

Nutrition, Cancer Genetics and Epigenetics

Lundström¹

2019

obm genet

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Epidemiological data and meta-analysis have confirmed that there exists a strong association between nutrition and disease risk. In the context of cancer, it has been demonstrated that unhealthy diets increase the risk of disease. On the other hand, major dietary interventions and lifestyle changes have been demonstrated to provide therapeutic efficacy in cancer patients. Genetic mechanisms have been reported to be associated with cancer development induced by environmental and nutritional factors. Genetics plays an important role in the designing of personalized drugs and diets. Epigenetics has also been demonstrated to be affected by nutrition, leading to increased risk of disease when unhealthy diets are consumed, while healthy nutrition is able to provide both prophylactic and therapeutic efficacy.

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“…In this context of “environmental epigenetics,” the correlation between diet, epigenetics, and pancreatic cancer has been reviewed. 20 There is significant evidence that certain dietary factors are associated with pancreatic cancer, implying a role for epigenetic gene regulation. Several lifestyle factors have also been identified that might affect human health via epigenetic mechanisms.…”

mentioning

confidence: 99%

Histone Deacetylase Inhibition Restores Expression of Hypoxia-Inducible Protein NDRG1 in Pancreatic Cancer

Tiffon

2018

Pancreas

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ObjectivesN-myc downstream-regulated gene-1 (NDRG1) is a hypoxia-inducible and differentiation-related protein and candidate biomarker in pancreatic cancer. As NDRG1 expression is lost in high-grade tumors, the effects of the differentiating histone deacetylase inhibitor trichostatin A (TSA) were examined in human pancreatic cancer cell lines representing different tumor grades.MethodsPANC-1 (poorly differentiated) and Capan-1 (moderately to well-differentiated) cells were treated with TSA. Effects were assessed in vitro by microscopic analysis, colorimetric assays, cell counts, real-time polymerase chain reaction, and Western blotting.ResultsTreatment of PANC-1 cells over 4 days with 0.5 μM TSA restored cellular differentiation, inhibited proliferation, and enhanced p21Cip1 protein expression. Trichostatin A upregulated NDRG1 mRNA and protein levels under normoxia from day 1 and by 6-fold by day 4 (P < 0.01 at all time points). After 24 hours under hypoxia, NDRG1 expression was further increased in differentiated cells (P < 0.01). Favorable changes were identified in the expression of other hypoxia-regulated genes.ConclusionsHistone deacetylase inhibitors offer a potential novel epidrug approach for pancreatic cancer by reversing the undifferentiated phenotype and allowing patients to overcome resistance and better respond to conventional cytotoxic treatments.

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Nutrients and the Pancreas: An Epigenetic Perspective

Cited by 30 publications

References 89 publications

The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease

The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease

Nutrition, Cancer Genetics and Epigenetics

Histone Deacetylase Inhibition Restores Expression of Hypoxia-Inducible Protein NDRG1 in Pancreatic Cancer

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