Despite several epidemiologic and preclinical studies supporting the role of diet in cancer progression, the complexity of the diet–cancer link makes it challenging to deconvolute the underlying mechanisms, which remain scantly elucidated. This review focuses on genomic instability as one of the cancer hallmarks affected by diet-dependent metabolic alterations. We discuss how altered dietary intake of metabolites of the one-carbon metabolism, including methionine, folate, and vitamins B and C, can impact the methylation processes and thereby tumorigenesis. We present the concept that the protumorigenic effect of certain diets, such as the Western diet, is in part due to a diet-induced erosion of the DNA repair capacity caused by altered epigenetic and epitranscriptomic landscapes, while the protective effect of other dietary patterns, such as the Mediterranean diet, can be partly explained by their ability to sustain a proficient DNA repair. In particular, considering that diet-dependent alterations of the one-carbon metabolism can impact the rate of methylation processes, changes in dietary patterns can affect the activity of writers and erasers of histone and RNA methyl marks and consequently impair their role in ensuring a proficient DNA damage repair.

中文翻译：

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癌症中 DNA 双链断裂修复的饮食依赖性代谢调节：菜单上有更多选择

尽管有几项流行病学和临床前研究支持饮食在癌症进展中的作用，但饮食与癌症之间联系的复杂性使得对潜在机制进行解卷积具有挑战性，而这些机制仍未得到充分阐明。这篇综述着重于基因组不稳定性作为受饮食依赖性代谢改变影响的癌症标志之一。我们讨论了单碳代谢代谢物（包括蛋氨酸、叶酸、维生素 B 和 C）的饮食摄入改变如何影响甲基化过程，从而影响肿瘤发生。我们提出这样一个概念，即某些饮食（例如西方饮食）的促癌作用部分是由于饮食引起的 DNA 修复能力的侵蚀，这是由改变的表观遗传和表观转录组景观引起的，而其他饮食模式的保护作用，例如地中海饮食，可以部分解释为它们维持熟练的 DNA 修复的能力。特别是，考虑到单碳代谢的饮食依赖性改变会影响甲基化过程的速率，饮食模式的变化会影响组蛋白和 RNA 甲基标记的书写者和擦除者的活动，从而削弱它们在确保熟练掌握DNA损伤修复。