Copper exerts cytotoxicity through inhibition of iron-sulfur cluster biogenesis on ISCA1/ISCA2/ISCU assembly proteins

Du, Jing; Huang, Zhaoyang; Li, Yanchun; Ren, Xueying; Zhou, Chunhui; Liu, Ruolan; Zhang, Ping; Lei, Guojie; Lyu, Jianxin; Li, Jianghui; Tan, Guoqiang

doi:10.1016/j.freeradbiomed.2023.05.017

Cited by 10 publications

(2 citation statements)

References 56 publications

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“…In the current work, DSF/Cu significantly initiated cuproptosis with down-regulation of iron-sulfur proteins and FDX1. Our recent paper demonstrated that human ISCA1, ISCA2 and ISCU proteins harbor strong copper-binding activity, which would impair Fe–S assembly [ 72 ]. These observations may be the potential mechanism for the reduced iron-sulfur proteins in the process of cuproptosis.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting the compensatory elevation of xCT collaborates with disulfiram/copper-induced GSH consumption for cascade ferroptosis and cuproptosis

Zhang,

Zhou,

Ren

et al. 2024

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Inhibiting the compensatory elevation of xCT collaborates with disulfiram/copper-induced GSH consumption for cascade ferroptosis and cuproptosis

Zhang,

Zhou,

Ren

et al. 2024

Redox Biology

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“…Although cuprotosis is associated with reduced levels of Fe-S cluster proteins, their role in HCC remains elusive. Moreover, Fe-S cluster biogenesis may be a primary target of copper toxicity [66]. Thus, further understanding of impaired Fe-S clusters can help to develop latent therapeutic strategies for the management of cancer [67].…”

Section: The Role Of Copper In Carcinogenesismentioning

confidence: 99%

The mechanism of copper homeostasis and its role in disease

Liang

Chen

et al. 2023

iLABMED

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Copper (Cuprum) is an essential trace metal indispensable for the function of numerous enzymatic molecules implicated in cellular metabolism. Emerging evidence has demonstrated the role of copper in angiogenesis and cellular signaling. Moreover, raised copper levels have been detected in hepatocellular carcinoma and other cancers. An inherited or acquired copper imbalance, including inadequately low or excessively high copper levels, as well as inappropriate copper distribution in the body, is implicated in a number of diseases. In addition, a recent groundbreaking study identified a copper‐induced type of programmed cell death named cuprotosis, the mechanism of which greatly deferred from that of other known cell death modes. The first part provides an overview of the regulation of copper homeostasis and discusses the underlying mechanisms of cuprotosis. In the second part, the authors focus on the functions of copper in liver diseases and other metabolic disorders, before discussing how this knowledge could contribute to the development of effective targets to treat such diseases.

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Alleviation of Copper-Induced Hepatotoxicity by Bergenin: Diminution of Oxidative Stress, Inflammation, and Apoptosis via Targeting SIRT1/FOXO3a/NF-κB Axes and p38 MAPK Signaling

Alanazi,

Salama,

Althobaiti

et al. 2024

Biol Trace Elem Res

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Copper exerts cytotoxicity through inhibition of iron-sulfur cluster biogenesis on ISCA1/ISCA2/ISCU assembly proteins

Cited by 10 publications

References 56 publications

Inhibiting the compensatory elevation of xCT collaborates with disulfiram/copper-induced GSH consumption for cascade ferroptosis and cuproptosis

Inhibiting the compensatory elevation of xCT collaborates with disulfiram/copper-induced GSH consumption for cascade ferroptosis and cuproptosis

The mechanism of copper homeostasis and its role in disease

Alleviation of Copper-Induced Hepatotoxicity by Bergenin: Diminution of Oxidative Stress, Inflammation, and Apoptosis via Targeting SIRT1/FOXO3a/NF-κB Axes and p38 MAPK Signaling

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