Biomineralized CO gas-releasing nanoprodrug for endoplasmic reticulum stress mediated cancer therapy

Gu, Rui; Yang, Wanlan; Han, Lina; Liu, Chao; Xu, Yatao; Liu, Yunlong; Si, Weili; Wang, Wenjun; Dong, Xiaochen

doi:10.1007/s12274-023-5458-8

Cited by 4 publications

(3 citation statements)

References 30 publications

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“…Cell homeostasis relies on proper mitochondrial functioning, making it crucial to closely monitor any potential damage to mitochondria. [ 43 ] The JC‐1 probe was used to monitor the change of mitochondrial membrane potential. Figure 4d demonstrates that the mitochondrial membrane potential was disrupted to different extents in all treatment groups.…”

Section: Resultsmentioning

confidence: 99%

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

Ding,

Wei,

Fang

et al. 2024

Adv Funct Materials

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Hydrogen sulfide (H2S) is being progressively integrated as an emerging inhibitor of the electron transport chain in energy interference‐based tumor therapy. However, metabolic reprogramming in cancer cells causes both oxidative phosphorylation (OXPHOS) and glycolysis to occur simultaneously, which contributes to the ineffective therapeutic effect of blocking a single pathway. To achieve complete suppression of energy production, an inorganic H2S donor ZnS@ZIF‐8@CaP nanoparticle (ZSZC NP) carrying Ca and Zn is constructed for achieving simultaneous interference of OXPHOS and glycolysis. The core–shell ZSZC nanoparticles can break down in the tumor microenvironment. This leads to a sustained H2S release and calcium overload to disrupt the normal functioning of mitochondria by inhibiting the expression of cytochrome c and causing damage to mitochondrial membrane potential. Meanwhile, the presence of Zn2+ hinders the typical process of glycolysis by impeding the functioning of lactate dehydrogenase and glyceraldehyde‐3‐phosphate dehydrogenase. The synchronous interference of OXPHOS and glycolysis hampers the energy supply to cancer cells. Additionally, H2S and calcium overload can expedite tumor necrosis in vivo by inducing cellular acidification and calcification. Therefore, this energy‐blocking strategy will completely deplete the energy reserves of cancer cells and provide new insights for exploring bioenergetic inhibition as a treatment approach.

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Section: Resultsmentioning

confidence: 99%

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

Ding,

Wei,

Fang

et al. 2024

Adv Funct Materials

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“…Therefore, safe CO prodrugs 3,4 and CO-releasing molecules (CORMs) were developed. [40][41][42][43] First-generation CORMs are transition-metal carbonyl complexes; however, they are toxic and the release of CO is uncontrollable. 5 Therefore, metal-free small molecular organic CORMs, especially photoactivated CORMs, namely photoCORMs, were developed.…”

Section: Introductionmentioning

confidence: 99%

Exactly controlled linear CO liberation: an A- and B-ring simultaneously extended flavonol-based red fluorescent photoCORM

Zhang

Sun

et al. 2023

Org. Biomol. Chem.

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“…[12][13][14] To this end, many efforts have been devoted to impairing mitochondrial function through CO-mediated gas therapy, which has great potential in combating chemotherapy-resistant tumors. [15][16][17][18][19][20] In another aspect, in normal conditions, the calcium buffering capacity of mitochondria can elaborately regulate the level of intracellular calcium, which is indispensable for cell energetics by activating oxidative metabolism, mitochondrial respiration, and ATP synthesis. [21,22] Under special circumstances, extreme levels of Ca 2+ beyond the mitochondrial calcium retention capacity may lead to reduced ATP production and the increased release of ROS.…”

Section: Introductionmentioning

confidence: 99%

Vacancy‐Rich Bismuth‐Based Nanosheets for Mitochondrial Destruction via CO Poisoning, Ca²⁺ Dyshomeostasis, and Oxidative Damage

Zhao,

Wang,

et al. 2023

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Mitochondria are core regulators of tumor cell homeostasis, and their damage has become an arresting therapeutic modality against cancer. Despite the development of many mitochondrial‐targeted pharmaceutical agents, the exploration of more powerful and multifunctional medications is still underway. Herein, oxygen vacancy‐rich BiO2‐x wrapped with CaCO3 (named BiO2‐x@CaCO3/PEG, BCP) is developed for full‐fledged attack on mitochondrial function. After endocytosis of BCP by tumor cells, the CaCO3 shell can be decomposed in the acidic lysosomal compartment, leading to immediate Ca2+ release and CO2 production in the cytoplasm. Near‐infrared irradiation enhances the adsorption of CO2 onto BiO2‐x defects, which enables highly efficient photocatalysis of CO2‐to‐CO. Meanwhile, such BiO2‐x nanosheets possess catalase‐, peroxidase‐ and oxidase‐like catalytic activities under acidic pH conditions, allowing hypoxia relief and the accumulation of diverse reactive oxygen species (ROS) in the tumor microenvironment. Ca2+ overload‐induced ion dyshomeostasis, CO‐mediated respiratory chain poisoning, ROS‐triggered oxidative stress aggravation, and cytosolic hyperoxia can cause severe mitochondrial disorders, which further lead to type I cell death in carcinoma. Not only does BCP cause irreversible apoptosis, but immunogenic cell death is simultaneously triggered to activate antitumor immunity for metastasis inhibition. Collectively, this platform promises high benefits in malignant tumor therapy and may expand the medical applications of bismuth‐based nanoagents.

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Biomineralized CO gas-releasing nanoprodrug for endoplasmic reticulum stress mediated cancer therapy

Cited by 4 publications

References 30 publications

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

Exactly controlled linear CO liberation: an A- and B-ring simultaneously extended flavonol-based red fluorescent photoCORM

Vacancy‐Rich Bismuth‐Based Nanosheets for Mitochondrial Destruction via CO Poisoning, Ca²⁺ Dyshomeostasis, and Oxidative Damage

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Biomineralized CO gas-releasing nanoprodrug for endoplasmic reticulum stress mediated cancer therapy

Cited by 4 publications

References 30 publications

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

A Multichannel Metabolic Pathway Interference Strategy for Complete Energy Depletion‐Mediated Cancer Therapy

Exactly controlled linear CO liberation: an A- and B-ring simultaneously extended flavonol-based red fluorescent photoCORM

Vacancy‐Rich Bismuth‐Based Nanosheets for Mitochondrial Destruction via CO Poisoning, Ca2+ Dyshomeostasis, and Oxidative Damage

Contact Info

Product

Resources

About

Vacancy‐Rich Bismuth‐Based Nanosheets for Mitochondrial Destruction via CO Poisoning, Ca²⁺ Dyshomeostasis, and Oxidative Damage