'Dormancy', in the context of carcinogenesis, is a biological phenomenon of decreased cancer cell proliferation and metabolism. In view of their ability to remain quiescent, cancer cells are able to avoid cell death induced by chemotherapeutic agents, and thereby give rise to tumor relapse at a later stage. Being a dynamic event, the dormant state is controlled by several epigenetic mechanisms, including the action of microRNAs. The present review highlights microRNAs that have been shown to be dysregulated in dormant cancer cells among different tumor types. MicroRNAs accomplish their control of cancer cell quiescence by targeting cell cycle regulators and signaling pathways involved in cell growth maintenance, including the AKT/phosphoinositide 3-kinase (PI3K) pathway. MicroRNAs, as components of intercellular vesicles, enable interactions to occur between cancer cells and cells of the microenvironment, resulting in the cancer cells either acquiring the quiescent state or, oppositely, stimulating them to proliferate. Taken together, the evidence obtained to date has collectively confirmed the involvement of microRNAsin cancer cell dormancy. Modulation of the various processes may enable optimization of the treatment of metastatic tumors.

中文翻译：

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MicroRNA对癌细胞休眠的控制。

在致癌作用中，“休眠”是降低癌细胞增殖和代谢的生物学现象。考虑到它们保持静止的能力，癌细胞能够避免由化学治疗剂诱导的细胞死亡，从而在以后的阶段引起肿瘤复发。作为动态事件，休眠状态受几种表观遗传机制控制，包括microRNA的作用。本综述重点介绍了已显示在不同肿瘤类型之间的休眠癌细胞中失调的microRNA。MicroRNA通过靶向细胞周期调节剂和参与细胞生长维持的信号传导途径（包括AKT /磷酸肌醇3-激酶（PI3K）途径）来实现对癌细胞休眠的控制。MicroRNA作为细胞间小泡的成分，使癌细胞与微环境细胞之间发生相互作用，导致癌细胞获得静止状态或相反地刺激它们增殖。综上所述，迄今为止获得的证据已共同证实了microRNAs参与了癌细胞的休眠。各种过程的调节可以使转移性肿瘤的治疗最优化。