肿瘤是起源于各种器官或组织的异质细胞团。肿瘤细胞团的细胞组成以复杂的方式相互作用，受到决定肿瘤生长或抑制的体液、遗传、分子和肿瘤微环境线索的影响。因此，肿瘤在临床可辨别的阶段之前经历一段休眠状态，这超过了临床休眠阈值。此外，作为一种基因印记策略，早期播种细胞（一种独特的肿瘤细胞群）会断裂并停靠在附近或渗入血管至次生组织，在那里它们形成具有可逆能力的播散性孤立休眠肿瘤细胞。在休眠肿瘤块和休眠肿瘤细胞形成的各种机制中，热休克蛋白（HSP）可能在休眠程序的发挥中发挥最重要的作用之一。众所周知，许多异常的细胞过程，例如恶性转化、癌细胞干性、肿瘤侵袭、转移、血管生成和信号通路维持，都受到HSP的影响。不断积累的知识表明，HSP 可能参与血管生成开关、免疫编辑和细胞外基质 (ECM) 重塑级联，这​​些对肿瘤休眠启动和休眠维持程序很重要的关键遗传印记策略。在这篇综述中，我们重点介绍了协调休眠状态的生物事件以及针对肿瘤块中热休克蛋白动态以及肿瘤细胞休眠和重新激活进行的工作。此外，我们提出了一个概念框架，该框架可能是转移性复发中休眠肿瘤重新激活的基础。

Tumors are a heterogeneous group of cell masses originating in various organs or tissues. The cellular composition of the tumor cell mass interacts in an intricate manner, influenced by humoral, genetic, molecular, and tumor microenvironment cues that dictate tumor growth or suppression. As a result, tumors undergo a period of a dormant state before their clinically discernible stage, which surpasses the clinical dormancy threshold. Moreover, as a genetically imprinted strategy, early-seeder cells, a distinct population of tumor cells, break off to dock nearby or extravasate into blood vessels to secondary tissues, where they form disseminated solitary dormant tumor cells with reversible capacity. Among the various mechanisms underlying the dormant tumor mass and dormant tumor cell formation, heat shock proteins (HSPs) might play one of the most important roles in how the dormancy program plays out. It is known that numerous aberrant cellular processes, such as malignant transformation, cancer cell stemness, tumor invasion, metastasis, angiogenesis, and signaling pathway maintenance, are influenced by the HSPs. An accumulating body of knowledge suggests that HSPs may be involved in the angiogenic switch, immune editing, and extracellular matrix (ECM) remodeling cascades, crucial genetically imprinted strategies important to the tumor dormancy initiation and dormancy maintenance program. In this review, we highlight the biological events that orchestrate the dormancy state and the body of work that has been conducted on the dynamics of HSPs in a tumor mass, as well as tumor cell dormancy and reactivation. Additionally, we propose a conceptual framework that could possibly underlie dormant tumor reactivation in metastatic relapse.