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dc.contributor.author | Vong K. | |
dc.contributor.author | Tahara T. | |
dc.contributor.author | Urano S. | |
dc.contributor.author | Nasibullin I. | |
dc.contributor.author | Tsubokura K. | |
dc.contributor.author | Nakao Y. | |
dc.contributor.author | Kurbangalieva A. | |
dc.contributor.author | Onoe H. | |
dc.contributor.author | Watanabe Y. | |
dc.contributor.author | Tanaka K. | |
dc.date.accessioned | 2022-02-09T20:45:34Z | |
dc.date.available | 2022-02-09T20:45:34Z | |
dc.date.issued | 2021 | |
dc.identifier.uri | https://dspace.kpfu.ru/xmlui/handle/net/170084 | |
dc.description.abstract | This study presents the early framework of selective cell tagging (SeCT) therapy, which is the concept of preferentially labeling specific cells in vivo with chemical moieties that can elicit a therapeutic response. Using glycosylated artificial metalloenzyme (GArM)-based protein labeling, this study reports two separate functional strategies. In one approach, early tumor onset can be suppressed by tagging cancer cells in living mice with an integrin-blocking cyclic-Arg-Gly-Asp (cRGD) moiety, thereby disrupting cell adhesion onto the extracellular matrix. In another approach, tumor growth in mice can be reduced by tagging with a cytotoxic doxorubicin moiety. Subsequent cell death occurs following internalization and drug release. Overall, experiments have shown that mouse populations receiving the mixture of SeCT labeling reagents exhibited a significant delay/reduction in tumor onset and growth compared with controls. Highlighting its adaptability, this work represents a foundational step for further development of SeCT therapy and its potential therapeutic applications. | |
dc.title | Disrupting tumor onset and growth via selective cell tagging (SeCT) therapy | |
dc.type | Article | |
dc.relation.ispartofseries-issue | 17 | |
dc.relation.ispartofseries-volume | 7 | |
dc.collection | Публикации сотрудников КФУ | |
dc.source.id | SCOPUS-2021-7-17-SID85105105749 |