Recent advances in enhancing reactive oxygen species based chemodynamic therapy

Li, Xinchao; Luo, Rui; Liang, Xiuqi; Wu, Qinjie; Gong, Changyang

doi:10.1016/j.cclet.2021.11.048

Cited by 42 publications

(24 citation statements)

References 154 publications

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“…Inhibiting GPX4 activity can lead to LPO accumulation, a significant feature of ferroptosis (Wei et al, 2020 ; Tang et al, 2021 ). In addition, studies have also confirmed that direct targeting of GPX4 is more effective than the destruction of GSH in cancer treatment based on ferroptosis (Shintoku et al, 2017 ; X. Li et al, 2022 ). Methyl (1 S ,3 R )-2-(2-chloroacetyl)-1-(4-(methoxycarbonyl)phenyl)-2,3,4,9-tetrahydro-1 H -pyrido[3,4- b ]indole-3-carboxylate (RSL-3) contains electrophilic chloroacetamide moiety, which irreversibly binds to its active site, directly inhibiting the catalytic activity of GPX4 (Eaton et al, 2020 ).…”

Section: Introductionmentioning

confidence: 92%

‘Mito-Bomb’: a novel mitochondria-targeting nanosystem for ferroptosis-boosted sonodynamic antitumor therapy

et al. 2022

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Mitochondria play an important role in regulating tumor cell death and metabolism so that they can be potential therapeutic targets. Sonodynamic therapy (SDT) represents an attractive antitumor method that induces apoptosis by producing highly toxic reactive oxygen species (ROS). Mitochondria-targeting SDT can cause oxidative damage and improve the efficiency of tumor therapy. However, due to the nonselective distribution of nanosystems and the anti-apoptotic mechanism of cancer cells, the therapeutic effect of SDT is not ideal. Therefore, we proposed a novel mitochondria-targeting nanosystem (‘Mito-Bomb’) for ferroptosis-boosted SDT. Sonosensitizer IR780 and ferroptosis activator RSL-3 were both encapsulated in biocompatible poly(lactic‐ co ‐glycolic acid) (PLGA) nanoparticles to form ‘Mito-Bomb’ (named IRP NPs). IR780 in this nanosystem was used to mediate mitochondria-targeting SDT. RSL-3 inhibited the activity of GPX4 in the antioxidant system to induce ferroptosis of tumor cells, which could rewire tumor metabolism and make tumor cells extremely sensitive to SDT-induced apoptosis. Notably, we also found that RSL-3 can inhibit hypoxia inducible factor-1α (HIF-1α) and induce ROS production to improve the efficacy of SDT to synergistically antitumor. RSL-3 was applied as a ‘One-Stone-Three-Birds’ agent for cooperatively enhanced SDT against triple-negative breast cancer. This study presented the first example of RSL-3 boosting mitochondria-targeting SDT as a ferroptosis activator. The ‘Mito-Bomb’ biocompatible nanosystem was expected to become an innovative tumor treatment method and clinical transformation.

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Section: Introductionmentioning

confidence: 92%

‘Mito-Bomb’: a novel mitochondria-targeting nanosystem for ferroptosis-boosted sonodynamic antitumor therapy

et al. 2022

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“…However, these particles were not stable in aqueous media, and their reaction was not efficient, most of which occurred only on the particle surfaces 11–13 . Moreover, even in the presence of Fe ions, endogenous H 2 O 2 , albeit higher in cancer environments, is not yet sufficient to generate therapeutic levels of ROS that effectively kill cancer cells, resulting in low treatment efficacy 14,15 …”

Section: Introductionmentioning

confidence: 99%

Fe‐containing metal–organic framework with D‐penicillamine for cancer‐specific hydrogen peroxide generation and enhanced chemodynamic therapy

Kim

Min

et al. 2023

Bioengineering & Transla Med

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Chemodynamic therapy (CDT) is based on the production of cytotoxic reactive oxygen species, such as hydroxyl radicals (•OH). Thus, CDT can be advantageous when it is cancer‐specific, in terms of efficacy and safety. Therefore, we propose NH2‐MIL‐101(Fe), a Fe‐containing metal–organic framework (MOF), as a carrier of Cu (copper)‐chelating agent, d‐penicillamine (d‐pen; i.e., the NH2‐MIL‐101(Fe)/d‐pen), as well as a catalyst with Fe‐metal clusters for Fenton reaction. NH2‐MIL‐101(Fe)/d‐pen in the form of nanoparticles was efficiently taken into cancer cells and released d‐pen in a sustained manner. The released d‐pen chelated Cu that is highly expressed in cancer environments and this produces extra H2O2, which is then decomposed by Fe in NH2‐MIL‐101(Fe) to generate •OH. Therefore, the cytotoxicity of NH2‐MIL‐101(Fe)/d‐pen was observed in cancer cells, not in normal cells. We also suggest a formulation of NH2‐MIL‐101(Fe)/d‐pen combined with NH2‐MIL‐101(Fe) loaded with the chemotherapeutic drug, irinotecan (CPT‐11; NH2‐MIL‐101(Fe)/CPT‐11). When intratumorally injected into tumor‐bearing mice in vivo, this combined formulation exhibited the most prominent anticancer effects among all tested formulations, owing to the synergistic effect of CDT and chemotherapy.

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“…17,18 Although some substantial efforts have revealed that the H 2 O 2 abundance in cancer cells is higher than that in normal cells, its abundance is insufficient to generate adequate ˙OH by Fenton-like reactions for amplifying oxidative stress in the TME. 19,20 Recently, to settle this point of inadequate H 2 O 2 , a large number of studies have been directed toward the delivery of exogenous H 2 O 2 , 21 amplification of endogenous H 2 O 2 , 22 or decomposition of metal peroxides. 23 For example, natural glucose oxidase as a kind of H 2 O 2 producer can greatly amplify H 2 O 2 abundance in the TME.…”

Section: Introductionmentioning

confidence: 99%

TME-triggered copper-coordinated engineered programmable nanogenerators for on-demand cascade-amplifying oxidative stress

Huang

Wang

et al. 2023

J. Mater. Chem. B

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Recent advances in enhancing reactive oxygen species based chemodynamic therapy

Cited by 42 publications

References 154 publications

‘Mito-Bomb’: a novel mitochondria-targeting nanosystem for ferroptosis-boosted sonodynamic antitumor therapy

‘Mito-Bomb’: a novel mitochondria-targeting nanosystem for ferroptosis-boosted sonodynamic antitumor therapy

Fe‐containing metal–organic framework with D‐penicillamine for cancer‐specific hydrogen peroxide generation and enhanced chemodynamic therapy

TME-triggered copper-coordinated engineered programmable nanogenerators for on-demand cascade-amplifying oxidative stress

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