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NO-dependent vasodilation and deep tumor penetration for cascade-amplified antitumor performance

Xu, Qing, Chen, Gui, Chen, Guimei, Wu, Hualan, Yang, Yuanyuan, Mai, Ziyi, Sun, Rui, Luan, Ping, Guo, Chaowan, Yu, Meng, Peng, Zhenwei, Yu, Zhiqiang·2022·Journal of Controlled Release
DOI 10.1016/j.jconrel.2022.05.022
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Abstract

Nonspecific biodistribution and poor permeability of conventional therapeutic agents in solid tumors severely compromised the antitumor efficacy. Herein, we report a cascade tumor therapeutic nanoplatform consisting of docosahexaenoic acid (DHA) and nicorandil (NI), namely DNP, to specifically produce cytotoxic agents in tumor cells as well as dilating blood vessels to increase the intratumoral oxidative stress levels. The DHA embedded in the membrane could generate reactive oxygen species (ROS) meanwhile NI produced nitric oxide (NO) in response to intracellular glutathione (GSH) in tumors. Notably, the two functional species could further react in situ to form a more tumoricidal reactive nitrogen species (RNS), causing selectively cascade amplification of antitumor performance. In addition, NO-induced vasodilation could consequently result in a series of functions, including hypoxia relief and deep tumor transportation. In general, we anticipate that the DNP could show great potential for tumor-specific treatment by selectively producing RNS precursors in response to the interior environment of tumor cells for hypoxia normalization and tumor inhibition.

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Metadata

Authors
Xu, Q., Chen, G., Chen, G., Wu, H., Yang, Y., Mai, Z., Sun, R., Luan, P., Guo, C., Yu, M., Peng, Z., & Yu, Z.
Venue
Journal of Controlled Release
Publisher
Elsevier BV
Published
2022-07
Volume
347
Pages
389-399
ISSN
0168-3659
DOI
10.1016/j.jconrel.2022.05.022
Cited by
35
References
2
Language
en
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