尽管 Hippo-YAP/TAZ 通路参与某些癌症的发展已被广泛研究，但该级联在肾癌进展中的参与尚未明确，因此将成为本综述的重点。肾细胞癌（RCC）是最常见的肾脏肿瘤亚型，预后差，死亡率高。核心 Hippo 信号失活（例如 LATS 激酶）导致 YAP/TAZ 核易位，在核易位中它们与共转录因子（例如 TEAD）结合，促进启动各种纤维化和肿瘤疾病的基因转录。 LATS1/2 激酶表达缺失和 YAP/TAZ 激活与 RCC 患者生存率低相关。小鼠中 LATS1 的肾脏特异性消融导致以 YAP/TAZ 依赖性方式自发发展几种 RCC 亚型。 YAP/TAZ 的遗传和药理学失活逆转了 LATS1 缺陷小鼠的致癌潜力，凸显了网络靶向在 RCC 中的治疗益处。在这里，我们探讨了肾癌中 Hippo-YAP/TAZ 通路失调的独特上游控制和下游后果。这篇综述批判性地评估了当前关于 Hippo 通路在 RCC 进展中的作用的文献，并强调了最近将 YAP/TAZ 指定为肾癌新治疗靶点的科学证据。

Although Hippo-YAP/TAZ pathway involvement has been extensively studied in the development of certain cancers, the involvement of this cascade in kidney cancer progression is not well-established and, therefore, will be the focus of this review. Renal cell carcinoma (RCC), the most prevalent kidney tumor subtype, has a poor prognosis and a high mortality rate. Core Hippo signaling inactivation (e.g., LATS kinases) leads to the nuclear translocation of YAP/TAZ where they bind to co-transcriptional factors such as TEAD promoting transcription of genes which initiates various fibrotic and neoplastic diseases. Loss of expression of LATS1/2 kinase and activation of YAP/TAZ correlates with poor survival in RCC patients. Renal-specific ablation of LATS1 in mice leads to the spontaneous development of several subtypes of RCC in a YAP/TAZ-dependent manner. Genetic and pharmacological inactivation of YAP/TAZ reverses the oncogenic potential in LATS1-deficient mice, highlighting the therapeutic benefit of network targeting in RCC. Here, we explore the unique upstream controls and downstream consequences of the Hippo-YAP/TAZ pathway deregulation in renal cancer. This review critically evaluates the current literature on the role of the Hippo pathway in RCC progression and highlights the recent scientific evidence designating YAP/TAZ as novel therapeutic targets against kidney cancer.