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首页> 外文期刊>Proceedings of the Nutrition Society >Epigenetic modifications and human pathologies: cancer and CVD.
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Epigenetic modifications and human pathologies: cancer and CVD.

机译：表观遗传修饰和人类病理学：癌症和CVD。

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摘要

Epigenetic changes are inherited alterations in DNA that affect gene expression and function without altering the DNA sequence. DNA methylation is one epigenetic process implicated in human disease that is influenced by diet. DNA methylation involves addition of a 1-C moiety to cytosine groups in DNA. Methylated genes are not transcribed or are transcribed at a reduced rate. Global under-methylation (hypomethylation) and site-specific over-methylation (hypermethylation) are common features of human tumours. DNA hypomethylation, leading to increased expression of specific proto-oncogenes (e.g. genes involved in proliferation or metastasis) can increase the risk of cancer as can hypermethylation and reduced expression of tumour suppressor (TS) genes (e.g. DNA repair genes). DNA methyltransferases (DNMT), together with the methyl donor S-adenosylmethionine (SAM), facilitate DNA methylation. Abnormal DNA methylation is implicated not only in the development of human cancer but also in CVD. Polyphenols, a group of phytochemicals consumed in significant amounts in the human diet, effect risk of cancer. Flavonoids from tea, soft fruits and soya are potent inhibitors of DNMT in vitro, capable of reversing hypermethylation and reactivating TS genes. Folates, a group of water-soluble B vitamins found in high concentration in green leafy vegetables, regulate DNA methylation through their ability to generate SAM. People who habitually consume the lowest level of folate or with the lowest blood folate concentrations have a significantly increased risk of developing several cancers and CVD. This review describes how flavonoids and folates in the human diet alter DNA methylation and may modify the risk of human colon cancer and CVD.
机译：表观遗传学改变是DNA的遗传改变，在不改变DNA序列的情况下影响基因表达和功能。 DNA甲基化是一种受饮食影响的人类疾病的表观遗传过程。 DNA甲基化涉及在DNA的胞嘧啶基团上添加一个1-C部分。甲基化的基因不被转录或以降低的速率被转录。总体甲基化不足（低甲基化）和位点特异性过度甲基化（高甲基化）是人类肿瘤的常见特征。 DNA甲基化过低会导致特定原癌基因（例如参与增殖或转移的基因）表达增加，而甲基化过高和肿瘤抑制（TS）基因（例如DNA修复基因）表达降低也会增加患癌症的风险。 DNA甲基转移酶（DNMT）与甲基供体S-腺苷甲硫氨酸（SAM）一起促进DNA甲基化。 DNA甲基化异常不仅与人类癌症的发展有关，而且与CVD有关。多酚是在人类饮食中大量消耗的一组植物化学物质，会致癌的风险。茶，软果和大豆中的类黄酮是DNMT体外的有效抑制剂，能够逆转高甲基化并激活TS基因。叶酸是在绿叶蔬菜中高浓度的一组水溶性B族维生素，它们通过产生SAM的能力来调节DNA甲基化。习惯性地摄入最低水平的叶酸或血液中的叶酸浓度最低的人患上几种癌症和CVD的风险显着增加。这篇评论描述了人类饮食中的类黄酮和叶酸如何改变DNA甲基化并可能改变人类结肠癌和CVD的风险。

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