Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202 (USA).
ChemMedChem. 2013 Dec;8(12):1963-77. doi: 10.1002/cmdc.201300340. Epub 2013 Oct 2.
The urokinase receptor (uPAR) is a cell-surface protein that is part of an intricate web of transient and tight protein interactions that promote cancer cell invasion and metastasis. Here, we evaluate the binding and biological activity of a new class of pyrrolidinone and piperidinone compounds, along with derivatives of previously-identified pyrazole and propylamine compounds. Competition assays revealed that the compounds displace a fluorescently labeled peptide (AE147-FAM) with inhibition constant (Ki ) values ranging from 6 to 63 μM. Structure-based computational pharmacophore analysis followed by extensive explicit-solvent molecular dynamics (MD) simulations and free energy calculations suggested the pyrazole-based and piperidinone-based compounds adopt different binding modes, despite their similar two-dimensional structures. In cells, pyrazole-based compounds showed significant inhibition of breast adenocarcinoma (MDA-MB-231) and pancreatic ductal adenocarcinoma (PDAC) cell proliferation, but piperidinone-containing compounds exhibited no cytotoxicity even at concentrations of 100 μM. One pyrazole-based compound impaired MDA-MB-231 invasion, adhesion, and migration in a concentration-dependent manner, while the piperidinone inhibited only invasion. The pyrazole derivative inhibited matrix metalloprotease-9 (gelatinase) activity in a concentration-dependent manner, while the piperidinone showed no effect suggesting different mechanisms for inhibition of cell invasion. Signaling studies further highlighted these differences, showing that pyrazole compounds completely inhibited ERK phosphorylation and impaired HIF1α and NF-κB signaling, while pyrrolidinones and piperidinones had no effect. Annexin V staining suggested that the effect of the pyrazole-based compound on proliferation was due to cell killing through an apoptotic mechanism. The compounds identified represent valuable leads in the design of further derivatives with higher affinities and potential probes to unravel the protein-protein interactions of uPAR.
尿激酶受体(uPAR)是一种细胞表面蛋白,它是一个复杂的瞬态和紧密蛋白相互作用网络的一部分,促进癌细胞的侵袭和转移。在这里,我们评估了一类新的吡咯烷酮和哌啶酮化合物,以及先前鉴定的吡唑和丙胺化合物的衍生物的结合和生物学活性。竞争测定表明,这些化合物以 6 至 63 μM 的抑制常数(Ki)值置换荧光标记肽(AE147-FAM)。基于结构的计算药效团分析,随后进行广泛的显式溶剂分子动力学(MD)模拟和自由能计算,表明基于吡唑的化合物和基于哌啶酮的化合物尽管具有相似的二维结构,但采用不同的结合模式。在细胞中,基于吡唑的化合物显著抑制乳腺癌(MDA-MB-231)和胰腺导管腺癌(PDAC)细胞的增殖,但含哌啶酮的化合物即使在 100 μM 的浓度下也没有细胞毒性。一种基于吡唑的化合物以浓度依赖的方式损害 MDA-MB-231 的侵袭、黏附和迁移,而哌啶酮仅抑制侵袭。吡唑衍生物以浓度依赖的方式抑制基质金属蛋白酶-9(明胶酶)活性,而哌啶酮则没有作用,表明抑制细胞侵袭的机制不同。信号研究进一步强调了这些差异,表明吡唑化合物完全抑制 ERK 磷酸化,并损害 HIF1α 和 NF-κB 信号,而吡咯烷酮和哌啶酮则没有影响。 Annexin V 染色表明,基于吡唑的化合物对增殖的影响是由于通过凋亡机制导致细胞杀伤。所鉴定的化合物代表了进一步设计具有更高亲和力和潜在探针的衍生物的有价值的先导物,以揭示 uPAR 的蛋白质-蛋白质相互作用。