Curbing Exosome Communications via Introducing Artificial Membrane Receptors for Metastatic Pancreatic Cancer Therapy
© 2023 Wiley-VCH GmbH.
| Veröffentlicht in: | Advanced materials (Deerfield Beach, Fla.). - 1998. - 35(2023), 39 vom: 07. Sept., Seite e2303736 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2023
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| Zugriff auf das übergeordnete Werk: | Advanced materials (Deerfield Beach, Fla.) |
| Schlagworte: | Journal Article bio-orthogonal click chemistry metabolic glycoengineering pancreatic cancer pre-metastatic niches tumor metastasis tumor-derived exosomes Membranes, Artificial |
| Zusammenfassung: | © 2023 Wiley-VCH GmbH. Tumor-derived exosomes (TDEs) carry various biomolecular cargos and play crucial roles in metastasis. TDEs migrate to distal organs for intercellular communication and induce the formation of pre-metastatic niches (PMNs) to support tumor implantation and proliferation. Precise interference in the bioprocess of TDEs is expected to be efficacious for suppressing tumor metastasis. However, targeting both TDEs and the primary tumor is challenging. Here, based on metabolic glycoengineering and bio-orthogonal click chemistry, a two-step delivery strategy is designed to overcome this. During the first step, the tetraacetylated N-azidoacetyl-d-mannosamine-loaded nanoparticle responds to the metabolic activity of tumor cells in the primary tumor, tagging both tumor cells and TDEs with azide groups; dibenzyl-cyclootyne-modified nanoparticles then can, as the second step, specifically react with tumor cells and TDEs through a bio-orthogonal click reaction. This strategy not only inhibits tumor growth in pancreatic cancer models but also curbs the communicative role of TDEs in inducing liver PMNs and metastasis by tracking and downregulating the exosomal macrophage migration inhibitory factor |
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| Beschreibung: | Date Completed 28.09.2023 Date Revised 28.09.2023 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-4095 |
| DOI: | 10.1002/adma.202303736 |