Lambert Lester J, Romero Celeste, Sheffler Douglas J, Celeridad Maria, Cosford Nicholas D P, Tautz Lutz
Cancer Metabolism & Signaling Networks Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute.
Cancer Metabolism & Signaling Networks Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute;
J Vis Exp. 2020 Jul 17(161). doi: 10.3791/61457.
The Src-homology 2 (SH2) domain-containing phosphatase 2 (SHP2), encoded by the PTPN11 proto-oncogene, is a key mediator of receptor tyrosine kinase (RTK)-driven cell signaling, promoting cell survival and proliferation. In addition, SHP2 is recruited by immune check point receptors to inhibit B and T cell activation. Aberrant SHP2 function has been implicated in the development, progression, and metastasis of many cancers. Indeed, small molecule SHP2 inhibitors have recently entered clinical trials for the treatment of solid tumors with Ras/Raf/ERK pathway activation, including tumors with some oncogenic Ras mutations. However, the current class of SHP2 inhibitors is not effective against the SHP2 oncogenic variants that occur frequently in leukemias, and the development of specific small molecules that target oncogenic SHP2 is the subject of current research. A common problem with most drug discovery campaigns involving cytosolic proteins like SHP2 is that the primary assays that drive chemical discovery are often in vitro assays that do not report the cellular target engagement of candidate compounds. To provide a platform for measuring cellular target engagement, we developed both wild-type and mutant SHP2 cellular thermal shift assays. These assays reliably detect target engagement of SHP2 inhibitors in cells. Here, we provide a comprehensive protocol of this assay, which provides a valuable tool for the assessment and characterization of SHP2 inhibitors.
由原癌基因PTPN11编码的含Src同源2(SH2)结构域的磷酸酶2(SHP2)是受体酪氨酸激酶(RTK)驱动的细胞信号传导的关键介质,可促进细胞存活和增殖。此外,免疫检查点受体可募集SHP2以抑制B细胞和T细胞的激活。SHP2功能异常与许多癌症的发生、发展和转移有关。事实上,小分子SHP2抑制剂最近已进入临床试验,用于治疗具有Ras/Raf/ERK途径激活的实体瘤,包括一些具有致癌性Ras突变的肿瘤。然而,目前这类SHP2抑制剂对白血病中频繁出现的SHP2致癌变体无效,开发靶向致癌性SHP2的特异性小分子是当前研究的主题。大多数涉及SHP2等胞质蛋白的药物发现活动的一个常见问题是,推动化学发现的主要检测方法通常是体外检测,无法报告候选化合物与细胞靶点的结合情况。为了提供一个测量细胞靶点结合的平台,我们开发了野生型和突变型SHP2细胞热位移检测方法。这些检测方法能够可靠地检测细胞中SHP2抑制剂与靶点的结合情况。在此,我们提供了该检测方法的全面方案,为评估和表征SHP2抑制剂提供了一个有价值的工具。