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Chemodynamic therapy (CDT), which employs intracellular H 2 O 2 to produce toxic hydroxyl radicals to kill cancer cells, has received great attention due to its specificity to tumors. However, the relatively insufficient endogenous H 2 O 2 and the short-lifetime and limited diffusion distance of •OH compromise the therapeutic efficacy of CDT. Mitochondria, which play crucial roles in oncogenesis, are highly vulnerable to elevated oxidative stress. Herein, we constructed a mitochondria-mediated self-cycling system to achieve high dose of •OH production through continuous H 2 O 2 supply. Cinnamaldehyde (CA), which can elevate H 2 O 2 level in the mitochondria, was loaded in Cu(II)-containing metal organic framework (MOF), termed as HKUST-1. After actively targeting mitochondria, the intrinsic H 2 O 2 in mitochondria of cancer cells could induce degradation of MOF, releasing the initial free CA. The released CA further triggered the upregulation of endogenous H 2 O 2 , resulting in the subsequent adequate release of CA and the final burst growth of H 2 O 2 . The cycle process greatly promoted the Fenton-like reaction between Cu 2+ and H 2 O 2 and induced long-term high oxidative stress, achieving enhanced chemodynamic therapy. In a word, we put forward an efficient strategy for enhanced chemodynamic therapy., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Metabolic glycan labeling (MGL) followed by bioorthogonal chemistry provides a powerful tool for tumor imaging and therapy. However, selectively metabolic labeling of cells or tissues of interest remains a challenge. Particularly, owing to tumor heterogeneity including tumor subtypes and interpatient heterogeneity, it is far more difficult to realize tumor-cell-selective metabolic labeling for precise diagnosis. Inspired by nature, we designed azidosugar-functionalized metal-organic frameworks camouflaged with cancer cell membranes to accomplish cancer-cell-selective MGL in vivo. With abundant receptors, this biomimetic platform not only selectively targets homotypic cells but also realizes different breast cancer subtype-selective MGL. Moreover, the endo/lysosomal-escaped ZIF-8 can make azidosugar escape from lysosomes and accelerate its metabolic incorporation. This strategy also takes advantage of cancer-tissue-derived cell membranes, which may have huge potential for personalized diagnosis and therapy., (© 2021 Wiley-VCH GmbH.)

Metabolic glycan labeling (MGL) followed by bioorthogonal chemistry provides a powerful tool for tumor imaging and therapy. However, selectively metabolic labeling of cells or tissues of interest remains a challenge. Particularly, owing to tumor heterogeneity including tumor subtypes and interpatient heterogeneity, it is far more difficult to realize tumor‐cell‐selective metabolic labeling for precise diagnosis. Inspired by nature, we designed azidosugar‐functionalized metal–organic frameworks camouflaged with cancer cell membranes to accomplish cancer‐cell‐selective MGL in vivo. With abundant receptors, this biomimetic platform not only selectively targets homotypic cells but also realizes different breast cancer subtype‐selective MGL. Moreover, the endo/lysosomal‐escaped ZIF‐8 can make azidosugar escape from lysosomes and accelerate its metabolic incorporation. This strategy also takes advantage of cancer‐tissue‐derived cell membranes, which may have huge potential for personalized diagnosis and therapy. [ABSTRACT FROM AUTHOR]