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Evaluation of Computationally Designed Peptides against TWEAK, a Cytokine of the Tumour Necrosis Factor Ligand Family.
Badia-Villanueva, Miriam; Defaus, Sira; Foj, Ruben; Andreu, David; Oliva, Baldo; Sierra, Angels; Fernandez-Fuentes, Narcis.
Afiliación
  • Badia-Villanueva M; Laboratory of Molecular and Translational Oncology, Centre de Recerca Biomèdica CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
  • Defaus S; Proteomics and Protein Chemistry Group, Department of Experimental and Health Science, Pompeu Fabra University, Barcelona, Biomedical Research Park, 08003 Barcelona, Spain.
  • Foj R; Laboratory of Molecular and Translational Oncology, Centre de Recerca Biomèdica CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
  • Andreu D; Proteomics and Protein Chemistry Group, Department of Experimental and Health Science, Pompeu Fabra University, Barcelona, Biomedical Research Park, 08003 Barcelona, Spain.
  • Oliva B; Structural Bioinformatics Lab (GRIB-IMIM), Department of Experimental and Health Science, Pompeu Fabra University, Biomedical Research Park, 08003 Barcelona, Spain.
  • Sierra A; Laboratory of Oncological Neurosurgery, Hospital Clinic de Barcelona-IDIBAPS, 08036 Barcelona, Spain.
  • Fernandez-Fuentes N; Department of Biosciences, U Science Tech, Universitat de Vic-Universitat Central de Catalunya, Vic 08500 Catalonia, Spain.
Int J Mol Sci ; 22(3)2021 Jan 21.
Article en En | MEDLINE | ID: mdl-33494438
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.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Péptidos / Diseño de Fármacos / Modelos Moleculares / Citocina TWEAK Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2021 Tipo del documento: Article País de afiliación: España

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Péptidos / Diseño de Fármacos / Modelos Moleculares / Citocina TWEAK Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2021 Tipo del documento: Article País de afiliación: España