DNA methylation dynamics in cellular commitment and differentiation

Suelves, Mònica; Carrió, Elvira; Núñez‐Álvarez, Yaiza; Peinado, Miguel A.

doi:10.1093/bfgp/elw017

Cited by 84 publications

(82 citation statements)

References 166 publications

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“…In diet-induced fatty liver, potentially compromised function of liverspecific enhancers attributed to elevated 5 mC, in combination with the ubiquitous loss of methylation at other developmentally repressed tissue-specific enhancers, may lead to cell de-differentiation, trans-differentiation, and loss of tissue identity events known to contribute to tumorigenesis. 27 FFC also recapitulated liver damage/tumor-triggered promoter hypermethylation events; genes in common were significantly enriched for carcinogenesis and developmental repression. More importantly, these hypermethylation events were reproducible in human HCC, suggesting conservation of at least some key epigenome deregulation events across species and etiology.…”

Section: Discussionmentioning

confidence: 93%

High fat diet and exercise lead to a disrupted and pathogenic DNA methylome in mouse liver

et al. 2016

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High-fat diet consumption and sedentary lifestyle elevates risk for obesity, non-alcoholic fatty liver disease, and cancer. Exercise training conveys health benefits in populations with or without these chronic conditions. Diet and exercise regulate gene expression by mediating epigenetic mechanisms in many tissues; however, such effects are poorly documented in the liver, a central metabolic organ. To dissect the consequences of diet and exercise on the liver epigenome, we measured DNA methylation, using reduced representation bisulfite sequencing, and transcription, using RNA-seq, in mice maintained on a fast food diet with sedentary lifestyle or exercise, compared with control diet with and without exercise. Our analyses reveal that genome-wide differential DNA methylation and expression of gene clusters are induced by diet and/or exercise. A combination of fast food and exercise triggers extensive gene alterations, with enrichment of carbohydrate/lipid metabolic pathways and muscle developmental processes. Through evaluation of putative protective effects of exercise on diet-induced DNA methylation, we show that hypermethylation is effectively prevented, especially at promoters and enhancers, whereas hypomethylation is only partially attenuated. We assessed diet-induced DNA methylation changes associated with liver cancer-related epigenetic modifications and identified significant increases at liver-specific enhancers in fast food groups, suggesting partial loss of liver cell identity. Hypermethylation at a subset of gene promoters was associated with inhibition of tissue development and promotion of carcinogenic processes. Our study demonstrates extensive reprogramming of the epigenome by diet and exercise, emphasizing the functional relevance of epigenetic mechanisms as an interface between lifestyle modifications and phenotypic alterations.

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Section: Discussionmentioning

confidence: 93%

High fat diet and exercise lead to a disrupted and pathogenic DNA methylome in mouse liver

et al. 2016

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“…This is frequently named as trained immunity [100], and gene expression is influenced by it. It does not require the participation of nervous system, as it is a typical cellular memory and consequently [101] it can be used by such single cells like unicellular animals or macrophages [102]. It uses the alteration of methylation pattern of genes, as a tool.…”

Section: Discussionmentioning

confidence: 99%

Complex multicellular functions at a unicellular eukaryote level: Learning, memory, and immunity

Csaba

2017

Acta Microbiologica et Immunologica Hungarica

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According to experimental data, eukaryote unicellulars are able to learn, have immunity and memory. Learning is carried out in a very primitive form, and the memory is not neural but an epigenetic one. However, this epigenetic memory, which is well justified by the presence and manifestation of hormonal imprinting, is strong and permanent in the life of cell and also in its progenies. This memory is epigenetically executed by the alteration and fixation of methylation pattern of genes without changes in base sequences. The immunity of unicellulars is based on self/non-self discrimination, which leads to the destruction of non-self invaders and utilization of them as nourishment (by phagocytosis). The tools of learning, memory, and immunity of unicellulars are uniformly found in plasma membrane receptors, which formed under the effect of dynamic receptor pattern generation, suggested by Koch et al., and this is the basis of hormonal imprinting, by which the encounter between a chemical substance and the cell is specifically memorized. The receptors and imprinting are also used in the later steps of evolution up to mammals (including man) in each mentioned functions. This means that learning, memory, and immunity can be deduced to a unicellular eukaryote level.

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“…Therefore, DNA methylation is a key player in the regulation of gene expression and is implicated in many cellular processes such as imprinting (Reik et al 1987, Swain et al 1987, X-chromosome inactivation (Mohandas et al 1981) and the establishment and maintenance of cell type-specific expression programs (reviewed in Suelves et al 2016). DNA methylation is also essential for the maintenance of genome stability by modeling chromatin structure (reviewed in Madakashira & Sadler 2017) as well as by silencing repetitive sequences to prevent chromosomal rearrangements (Gaudet et al 2003) and the expression and expansion of transposable elements (reviewed in Belancio et al 2010).…”

Section: What Is Dna Methylation?mentioning

confidence: 99%

DNA methylation in thyroid cancer

Zafón

Gil

Pérez-González

et al. 2019

Endocrine-Related Cancer

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In recent years, cancer genomics has provided new insights into genetic alterations and signaling pathways involved in thyroid cancer. However, the picture of the molecular landscape is not yet complete. DNA methylation, the most widely studied epigenetic mechanism, is altered in thyroid cancer. Recent technological advances have allowed the identification of novel differentially methylated regions, methylation signatures and potential biomarkers. However, despite recent progress in cataloging methylation alterations in thyroid cancer, many questions remain unanswered. The aim of this review is to comprehensively examine the current knowledge on DNA methylation in thyroid cancer and discuss its potential clinical applications. After providing a general overview of DNA methylation and its dysregulation in cancer, we carefully describe the aberrant methylation changes in thyroid cancer and relate them to methylation patterns, global hypomethylation and gene-specific alterations. We hope this review helps to accelerate the use of the diagnostic, prognostic and therapeutic potential of DNA methylation for the benefit of thyroid cancer patients.

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DNA methylation dynamics in cellular commitment and differentiation

Cited by 84 publications

References 166 publications

High fat diet and exercise lead to a disrupted and pathogenic DNA methylome in mouse liver

High fat diet and exercise lead to a disrupted and pathogenic DNA methylome in mouse liver

Complex multicellular functions at a unicellular eukaryote level: Learning, memory, and immunity

DNA methylation in thyroid cancer

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