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Involvement of Caveolin-1-mediated transcytosis in the intratumoral accumulation of liposomes

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Title: Involvement of Caveolin-1-mediated transcytosis in the intratumoral accumulation of liposomes
Authors: Sakurai, Yu Browse this author →KAKEN DB
Kato, Akari Browse this author
Harashima, Hideyoshi Browse this author →KAKEN DB
Keywords: EPR effect
Issue Date: 30-Apr-2020
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 525
Issue: 2
Start Page: 313
End Page: 318
Publisher DOI: 10.1016/j.bbrc.2020.02.086
Abstract: For achieving efficient cancer treatment, it is important to elucidate the mechanism responsible for the accumulation of nanoparticles in tumor tissue. Recent studies suggest that nanoparticles are not delivered merely through gaps between tumor endothelial cells. We previously reported that the maturation of the vascular structure by the vascular endothelial cell growth factor receptor 2 (VEGFR2) using a previously developed siRNA delivery technology (RGD-MEND) significantly enhanced the accumulation of nanoparticles in types of cancers that area vessel-rich (renal cell carcinoma). This result was completely inconsistent with the generally accepted theory of the enhanced permeability and retention (EPR) effect. We hypothesized that a caveolin-1 (Cav1)-mediated transcellular route would be involved with the penetration of nanoparticles into tumor vasculature. To reveal the exact mechanism responsible for this enhancement, we observed the delivery of long-circulating liposomes (LPs) after Cav1 was co-suppressed by RGD-MEND with VEGFR2. The enhanced delivery of LPs by siRNA against VEGFR2 (siVEGFR2) was accompanied by the elevated expression of the Cav1 protein. In addition, Cav1 knockdown by siRNA against Cav1 (siCav1) canceled the enhanced delivery of LPs by siVEGFR2. The injection of siCav1 had no effect on the formation of alpha smooth muscle actin or vascular endothelial cell adhesion molecules. These results suggest that a Cav1-induced transcellular route and not a paracellular route, at least partially, contributes to the accumulation of nanoparticles in tumors. (C) 2020 Elsevier Inc. All rights reserved.
Rights: ©2020. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 櫻井 遊

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