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 |
|