Legumain protease-activated TAT-liposome cargo for targeting tumours and their microenvironment

Ze Liu, Min Xiong, Junbo Gong, Yan Zhang, Nan Bai, Yunping Luo, Luyuan Li, Yuquan Wei, Yanhua Liu, Xiaoyue Tan () and Rong Xiang ()
Additional contact information
Ze Liu: Medical School of Nankai University, 94 Weijin Road
Min Xiong: Medical School of Nankai University, 94 Weijin Road
Junbo Gong: Tianjin Key Laboratory of Modern Drug Delivery and High Efficiency in Tianjin University, 92 Weijin Road
Yan Zhang: Medical School of Nankai University, 94 Weijin Road
Nan Bai: Medical School of Nankai University, 94 Weijin Road
Yunping Luo: Beijing Union Medical School, 5 Dong Dan San Tiao
Luyuan Li: Medical School of Nankai University, 94 Weijin Road
Yuquan Wei: State Key Laboratory of Biotherapy, West China Hospital, Sichuan University
Yanhua Liu: Medical School of Nankai University, 94 Weijin Road
Xiaoyue Tan: Medical School of Nankai University, 94 Weijin Road
Rong Xiang: Medical School of Nankai University, 94 Weijin Road

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract Specific targeting and cellular internalization are key properties for carriers of antitumor therapeutic agents. Here, we develop a drug carrier through the attachment of substrate of endoprotease legumain, alanine–alanine–asparagine (AAN), to cell-penetrating peptides (TAT, trans-activating factor). The addition of the AAN moiety to the fourth lysine in the TAT creates a branched peptide moiety, which leads to a decrease in the transmembrane transport capacity of TAT by 72.65%. Legumain efficiently catalyses the release of TAT-liposome from the AAN-TAT-liposome and thereby recovers the penetrating capacity of TAT. Doxorubicin carried by the AAN-TAT-liposome led to an increase in the tumoricidal effect of doxorubicin and a reduction in its systemic adverse effects in comparison with doxorubicin carried by a control delivery system. Thus, the specific targeting and high efficiency of this delivery platform offers a novel approach to limit the toxicity of anticancer agents as well as increasing their efficacy in cancer therapy.

Date: 2014
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms5280 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5280

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms5280

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().