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Gao, Fan; Dong, Jian‐Hui; Xue, Chun; Lu, Xin‐Xin; Cai, Yu; Tang, Zi‐Yang; Ou, Chang‐Jin
Small (Weinheim an der Bergstrasse, Germany), 06/2024, Volume: 20, Issue: 26Journal Article
Interfering with intratumoral metabolic processes is proven to effectively sensitize different antitumor treatments. Here, a tumor‐targeting catalytic nanoplatform (CQ@MIL‐GOX@PB) loading with autophagy inhibitor (chloroquine, CQ) and glucose oxidase (GOX) is fabricated to interfere with the metabolisms of tumor cells and tumor‐associated macrophages (TAMs), then realizing effective antitumor chemodynamic therapy (CDT). Once accumulating in the tumor site with the navigation of external biotin, CQ@MIL‐GOX@PB will release Fe ions and CQ in the acid lysosomes of tumor cells, the latter can sensitize Fe ions‐involved antitumor CDT by blocking the autophagy‐dependent cell repair. Meanwhile, the GOX component will consume glucose, which not only generates many H2O2 for CDT but also once again decelerates the tumor repair process by reducing energy metabolism. What is more, the release of CQ can also drive the NO anabolism of TAMs to further sensitize CDT. This strategy of multiple metabolic regulations is evidenced to significantly improve the antitumor effect of traditional CDT nanoagents and might provide a new sight to overcome the bottlenecks of different antitumor treatments. The tumor‐targeting multiple metabolic regulations are performed by the CQ@MIL‐GOX@PB nanosystem to achieve effective antitumor chemodynamic therapy (CDT). By promoting the NO anabolism of tumor‐associated macrophages, and inhibiting energy metabolism and autophagy of tumor cells, the CDT effect of CQ@MIL‐GOX@PB is burst via the multiple sensitization mechanisms.
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