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Disruption of the Molecular Circadian Clock and Cancer: An Epigenetic Link

机译：分子昼夜钟和癌症的破坏：表观遗传联系

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摘要

The circadian clock is regulated at the molecular level by feedback circuits of a group of genes known as "clock genes", which establish a mechanism that controls circadian cellular physiology to maintain the balance between cell proliferation, response to DNA damage and apoptosis. Alterations in the expression of clock genes due to genetic or epigenetic mechanisms have been associated with multiple diseases including cancer. Even some clock genes such as the Per1, Per2, Bmal1 genes have been proposed as tumor suppressor genes, with a relevant role during carcinogenesis. At the molecular level, multiple mechanisms of molecular control have been described to link circadian transcription, cell cycle control, and tumorigenesis. In addition, recent findings describe an epigenetic control of circadian transcription, at the level of DNA methylation as well as in the modifications of histones. However, the link between the circadian epigenome and cancer remains unclear. In this article, we review the evidence that suggests a relationship between alterations in the expression of clock genes, with the development of cancer, from the epigenetic landscape.
机译：昼夜节奏由一组称为“时钟基因”的基因的反馈电路调节，其建立一种控制昼夜细胞生理以维持细胞增殖之间平衡，对DNA损伤和凋亡的响应的机制。由于遗传或表观遗传机制引起的时钟基因表达的改变已经与包括癌症的多种疾病有关。甚至一些时钟基因，如PER1，PER2，BMA1基因已经被提出为肿瘤抑制基因，在致癌中具有相关的作用。在分子水平下，已经描述了多种分子对照机制来链接昼夜转录，细胞周期控制和肿瘤率。此外，最近的发现描述了昼夜转录的表观遗传控制，在DNA甲基化水平以及组蛋白的修饰中。然而，昼夜节律表观群组和癌症之间的联系仍然不清楚。在本文中，我们审查了表现出时钟基因表达的改变与癌症的发展之间的关系的证据。

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