Adjudin-loaded redox-sensitive paclitaxel-prodrug micelles for overcoming multidrug resistance with efficient targeted Colon cancer therapy

Multidrug resistance (MDR) is the primary cause for the failure of chemotherapy in the treatment of colon cancer. Recent research has indicated that the combination of a chemotherapeutic agent and a mitochondrial inhibitor might represent a promising strategy to help overcome MDR. However, for this...

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Main Authors: Deli Chen (Author), Sitang Ge (Author), Lugen Zuo (Author), Shuanhu Wang (Author), Mulin Liu (Author), Shiqing Li (Author)
Format: Book
Published: Taylor & Francis Group, 2020-01-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Deli Chen  |e author 
700 1 0 |a Sitang Ge  |e author 
700 1 0 |a Lugen Zuo  |e author 
700 1 0 |a Shuanhu Wang  |e author 
700 1 0 |a Mulin Liu  |e author 
700 1 0 |a Shiqing Li  |e author 
245 0 0 |a Adjudin-loaded redox-sensitive paclitaxel-prodrug micelles for overcoming multidrug resistance with efficient targeted Colon cancer therapy 
260 |b Taylor & Francis Group,   |c 2020-01-01T00:00:00Z. 
500 |a 1071-7544 
500 |a 1521-0464 
500 |a 10.1080/10717544.2020.1797245 
520 |a Multidrug resistance (MDR) is the primary cause for the failure of chemotherapy in the treatment of colon cancer. Recent research has indicated that the combination of a chemotherapeutic agent and a mitochondrial inhibitor might represent a promising strategy to help overcome MDR. However, for this approach to be clinically effective, it is important that the two drugs can be actively and simultaneously delivered into tumor cells at an optimal ratio and completely released drug within cells. To address these challenges, we designed and prepared a folate receptor-targeted and redox-responsive drug delivery system (FA-ss-P/A) that was able to co-deliver paclitaxel (PTX) and adjudin (ADD) to reverse colon cancer MDR. The PTX prodrug was obtained by conjugating PTX to dextrin via a disulfide-linkage. Then, folic acid (FA) was modified on the PTX prodrug. Finally, ADD, a mitochondrial inhibitor, was encapsulated in the PTX prodrug-formed micelles. A series of in vitro and in vivo experiments subsequently demonstrated that FA-ss-P/A can effectively reverse MDR by increasing cell uptake, inhibiting PTX efflux, and improving drug release. 
546 |a EN 
690 |a multidrug resistance 
690 |a co-delivery 
690 |a mitochondria-inhibition 
690 |a adjudin 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
655 7 |a article  |2 local 
786 0 |n Drug Delivery, Vol 27, Iss 1, Pp 1094-1105 (2020) 
787 0 |n http://dx.doi.org/10.1080/10717544.2020.1797245 
787 0 |n https://doaj.org/toc/1071-7544 
787 0 |n https://doaj.org/toc/1521-0464 
856 4 1 |u https://doaj.org/article/2802ee3d05c04be5a680004eafbde6e2  |z Connect to this object online.