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.

中文翻译：

---

分子生物钟和癌症的破坏：表观遗传学的联系。

通过称为“时钟基因”的一组基因的反馈回路在分子水平上调节生物钟，该生物钟建立了控制生物钟生理的机制，以维持细胞增殖，对DNA损伤的反应和细胞凋亡之间的平衡。由于遗传或表观遗传机制，时钟基因表达的改变与包括癌症在内的多种疾病有关。甚至有人提出了一些时钟基因，例如Per1，Per2，Bmal1基因作为抑癌基因，在致癌过程中具有重要作用。在分子水平上，已经描述了多种分子控制机制来联系昼夜节律转录，细胞周期控制和肿瘤发生。此外，最近的发现描述了生物钟转录的表观遗传控制，在DNA甲基化水平以及组蛋白修饰中。然而，昼夜节律表观基因组和癌症之间的联系仍然不清楚。在本文中，我们回顾了从表观遗传学角度提出时钟基因表达变化与癌症发生之间关系的证据。