Laboratory of Molecular and Translational Oncology, Centre de Recerca Biomèdica CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
Proteomics and Protein Chemistry Group, Department of Experimental and Health Science, Pompeu Fabra University, Barcelona, Biomedical Research Park, 08003 Barcelona, Spain.
Int J Mol Sci. 2021 Jan 21;22(3):1066. doi: 10.3390/ijms22031066.
The tumour necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumour necrosis factor ligand family and has been shown to be overexpressed in tumoral cells together with the fibroblast growth factor-inducible 14 (Fn14) receptor. TWEAK-Fn14 interaction triggers a set of intracellular pathways responsible for tumour cell invasion and migration, as well as proliferation and angiogenesis. Hence, modulation of the TWEAK-Fn14 interaction is an important therapeutic goal. The targeting of protein-protein interactions by external agents, e.g., drugs, remains a substantial challenge. Given their intrinsic features, as well as recent advances that improve their pharmacological profiles, peptides have arisen as promising agents in this regard. Here, we report, by in silico structural design validated by cell-based and in vitro assays, the discovery of four peptides able to target TWEAK. Our results show that, when added to TWEAK-dependent cellular cultures, peptides cause a down-regulation of genes that are part of TWEAK-Fn14 signalling pathway. The direct, physical interaction between the peptides and TWEAK was further elucidated in an in vitro assay which confirmed that the bioactivity shown in cell-based assays was due to the targeting of TWEAK. The results presented here are framed within early pre-clinical drug development and therefore these peptide hits represent a starting point for the development of novel therapeutic agents. Our approach exemplifies the powerful combination of in silico and experimental efforts to quickly identify peptides with desirable traits.
肿瘤坏死因子样凋亡弱诱导物(TWEAK)是肿瘤坏死因子配体家族的一员,已被证明在肿瘤细胞中与成纤维细胞生长因子诱导的 14 (Fn14)受体一起过表达。TWEAK-Fn14 相互作用触发了一组负责肿瘤细胞侵袭和迁移以及增殖和血管生成的细胞内途径。因此,调节 TWEAK-Fn14 相互作用是一个重要的治疗目标。通过外部剂(例如药物)靶向蛋白质-蛋白质相互作用仍然是一个重大挑战。鉴于它们的固有特征以及最近改善其药理学特征的进展,肽已成为这方面的有前途的药物。在这里,我们通过基于细胞的和体外测定验证的计算结构设计报告了发现四种能够靶向 TWEAK 的肽。我们的结果表明,当添加到依赖 TWEAK 的细胞培养物中时,肽会导致属于 TWEAK-Fn14 信号通路的基因下调。在体外测定中进一步阐明了肽与 TWEAK 之间的直接物理相互作用,该测定证实细胞测定中显示的生物活性是由于靶向 TWEAK。这里呈现的结果是在早期临床前药物开发的框架内进行的,因此这些肽是开发新型治疗剂的起点。我们的方法体现了计算和实验努力的强大结合,可快速识别具有理想特性的肽。