Tumor-Targeting Liposomes with Transient Holes Allowing Intact Rituximab Internally
DC Field | Value | Language |
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dc.contributor.author | Kim, Y. | - |
dc.contributor.author | Youn, Y.S. | - |
dc.contributor.author | Oh, K.T. | - |
dc.contributor.author | Kim, D. | - |
dc.contributor.author | Lee, E.S. | - |
dc.date.accessioned | 2021-12-16T02:41:36Z | - |
dc.date.available | 2021-12-16T02:41:36Z | - |
dc.date.issued | 2021-02 | - |
dc.identifier.issn | 1525-7797 | - |
dc.identifier.issn | 1526-4602 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/52504 | - |
dc.description.abstract | In this study, the strategy of transient generation of holes in the liposome surface has been shown to enable safe encapsulation of a high-molecular weight antibody (rituximab, Mw ∼140 kDa) within liposomes. These transient holes generated using our magnetoporation method allowed rituximab to safely enter the liposomes, and then the holes were plugged using hyaluronic acid grafted with 3-diethylaminopropylamine (DEAP). In the tumor microenvironment, the resulting liposomal rituximab was destabilized because of the ionization of the DEAP moiety at the acidic pH 6.5, resulting in extensive release of rituximab. Consequently, the rituximab released from the liposomes accumulated at high levels in tumors and bound to the CD20 receptors overexpressed on Burkitt lymphoma Ramos cells. This event led to significant enhancement in tumor cell ablation through rituximab-mediated complement-dependent cytotoxicity and Bcl-2 signaling inhibition-induced cell apoptosis. © 2020 American Chemical Society. | - |
dc.format.extent | 9 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | American Chemical Society | - |
dc.title | Tumor-Targeting Liposomes with Transient Holes Allowing Intact Rituximab Internally | - |
dc.type | Article | - |
dc.identifier.doi | 10.1021/acs.biomac.0c01514 | - |
dc.identifier.bibliographicCitation | Biomacromolecules, v.22, no.2, pp 723 - 731 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000618660700043 | - |
dc.identifier.scopusid | 2-s2.0-85097799714 | - |
dc.citation.endPage | 731 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 723 | - |
dc.citation.title | Biomacromolecules | - |
dc.citation.volume | 22 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordPlus | Cell death | - |
dc.subject.keywordPlus | Cell signaling | - |
dc.subject.keywordPlus | Cytotoxicity | - |
dc.subject.keywordPlus | Hyaluronic acid | - |
dc.subject.keywordPlus | Liposomes | - |
dc.subject.keywordPlus | Acidic pH | - |
dc.subject.keywordPlus | Cell apoptosis | - |
dc.subject.keywordPlus | Complement-dependent cytotoxicities | - |
dc.subject.keywordPlus | High molecular weight | - |
dc.subject.keywordPlus | Magnetoporation | - |
dc.subject.keywordPlus | Tumor cells | - |
dc.subject.keywordPlus | Tumor microenvironment | - |
dc.subject.keywordPlus | Tumor targeting | - |
dc.subject.keywordPlus | Tumors | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalResearchArea | Polymer Science | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Organic | - |
dc.relation.journalWebOfScienceCategory | Polymer Science | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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