Department of Biochemistry, School of Medicine, University of Occupational and Environmental Health, Fukuoka, Japan.
Division of Cancer Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Cancer Sci. 2024 Oct;115(10):3370-3383. doi: 10.1111/cas.16316. Epub 2024 Aug 18.
The activation of yes-associated protein 1 (YAP1) and transcriptional co-activator with PDZ-binding motif (TAZ) has been implicated in both regeneration and tumorigenesis, thus representing a double-edged sword in tissue homeostasis. However, how the activity of YAP1/TAZ is regulated or what leads to its dysregulation in these processes remains unknown. To explore the upstream stimuli modulating the cellular activity of YAP1/TAZ, we developed a highly sensitive YAP1/TAZ/TEAD-responsive DNA element (YRE) and incorporated it into a lentivirus-based reporter cell system to allow for sensitive and specific monitoring of the endogenous activity of YAP1/TAZ in terms of luciferase activity in vitro and Venus fluorescence in vivo. Furthermore, by replacing YRE with TCF- and NF-κB-binding DNA elements, we demonstrated the applicability of this reporter system to other pathways such as Wnt/β-catenin/TCF- and IL-1β/NF-κB-mediated signaling, respectively. The practicality of this system was evaluated by performing cell-based reporter screening of a chemical compound library consisting of 364 known inhibitors, using reporter-introduced cells capable of quantifying YAP1/TAZ- and β-catenin-mediated transcription activities, which led to the identification of multiple inhibitors, including previously known as well as novel modulators of these signaling pathways. We further confirmed that novel YAP1/TAZ modulators, such as potassium ionophores, Janus kinase inhibitors, platelet-derived growth factor receptor inhibitors, and genotoxic stress inducers, alter the protein level or phosphorylation of endogenous YAP1/TAZ and the expression of their target genes. Thus, this reporter system provides a powerful tool to monitor endogenous signaling activities of interest (even in living cells) and search for modulators in various cellular contexts.
Yes 相关蛋白 1(YAP1)和转录共激活因子与 PDZ 结合基序(TAZ)的激活与再生和肿瘤发生都有关,因此在组织稳态中代表了一把双刃剑。然而,YAP1/TAZ 的活性是如何调节的,或者在这些过程中导致其失调的原因是什么,目前尚不清楚。为了探索调节 YAP1/TAZ 细胞活性的上游刺激因素,我们开发了一种高度敏感的 YAP1/TAZ/TEAD 反应性 DNA 元件(YRE),并将其纳入基于慢病毒的报告细胞系统中,以允许在体外基于荧光素酶活性和体内 Venus 荧光的方式灵敏和特异性地监测 YAP1/TAZ 的内源性活性。此外,通过用 TCF 和 NF-κB 结合 DNA 元件替换 YRE,我们证明了该报告系统适用于其他途径,例如 Wnt/β-catenin/TCF 和 IL-1β/NF-κB 介导的信号转导。通过使用能够定量测定 YAP1/TAZ 和 β-catenin 介导的转录活性的报告细胞,对由 364 种已知抑制剂组成的化学化合物文库进行基于细胞的报告筛选,评估了该系统的实用性,这导致了多种抑制剂的鉴定,包括先前已知的以及这些信号通路的新型调节剂。我们进一步证实,新型 YAP1/TAZ 调节剂,如钾离子载体、Janus 激酶抑制剂、血小板衍生生长因子受体抑制剂和遗传毒性应激诱导剂,改变内源性 YAP1/TAZ 的蛋白水平或磷酸化及其靶基因的表达。因此,该报告系统为监测感兴趣的内源性信号活性(甚至在活细胞中)以及在各种细胞环境中寻找调节剂提供了一种强大的工具。