肿瘤休眠和复发性转移癌仍然是癌症患者面临的最大临床挑战。休眠的肿瘤细胞能够逃避治疗和检测，同时保留增殖潜力，并在疾病复发前经常保持数年的时间。细胞静止是一种促进和维持肿瘤休眠的机制，由于其在减少增殖、提高细胞保护机制和保留增殖潜力方面起着核心作用。静止/增殖决策受内在和外在信号的支配，这些信号通过调节细胞周期基因表达来调节细胞周期蛋白依赖激酶（CDKs）的活性。通过澄清调控CDK活性的途径和激活它们的信号，我们可以更好地了解癌细胞在休眠和转移性疾病进展过程中如何进入、维持和逃脱休眠状态。在这里，我们回顾了CDK活性调控细胞休眠的路径，并强调了它所带来的治疗挑战和机遇。© 2023. 作者(们)。

Tumour dormancy and recurrent metastatic cancer remain the greatest clinical challenge for cancer patients. Dormant tumour cells can evade treatment and detection, while retaining proliferative potential, often for years, before relapsing to tumour outgrowth. Cellular quiescence is one mechanism that promotes and maintains tumour dormancy due to its central role in reducing proliferation, elevating cyto-protective mechanisms, and retaining proliferative potential. Quiescence/proliferation decisions are dictated by intrinsic and extrinsic signals, which regulate the activity of cyclin-dependent kinases (CDKs) to modulate cell cycle gene expression. By clarifying the pathways regulating CDK activity and the signals which activate them, we can better understand how cancer cells enter, maintain, and escape from quiescence throughout the progression of dormancy and metastatic disease. Here we review how CDK activity is regulated to modulate cellular quiescence in the context of tumour dormancy and highlight the therapeutic challenges and opportunities it presents.© 2023. The Author(s).