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Review
. 2023 Feb 3;16(2):234.
doi: 10.3390/ph16020234.

"V体育官网入口" Potential of Copper and Copper Compounds for Anticancer Applications

Peng Ji  1 , Peng Wang  1 , Hao Chen  1 , Yajing Xu  1 , Jianwen Ge  1 , Zechong Tian  1 , Zhirong Yan  2
Affiliations
Review

"V体育官网入口" Potential of Copper and Copper Compounds for Anticancer Applications

Peng Ji et al. Pharmaceuticals (Basel). .

Abstract

Inducing cancer cell death has always been a research hotspot in life sciences. With the continuous deepening and diversification of related research, the potential value of metal elements in inducing cell death has been explored. Taking iron as an example, ferroptosis, mainly characterized by increasing iron load and driving the production of large amounts of lipid peroxides and eventually leading to cell death, has recently attracted great interest in the cancer research community. After iron, copper, a trace element, has received extensive attention in cell death, especially in inducing tumor cell death. Copper and its complexes can induce autophagy or apoptosis in tumor cells through a variety of different mechanisms of action (activation of stress pathways, arrest of cell cycle, inhibition of angiogenesis, cuproptosis, and paraptosis), which are promising in cancer therapy and have become new hotspots in cancer treatment research. This article reviews the main mechanisms and potential applications of novel copper and copper compound-induced cell death, focusing on copper compounds and their anticancer applications. VSports手机版.

Keywords: apoptosis; cancer; copper; copper compounds; oxidative stress; reactive oxygen species. V体育安卓版.

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"V体育2025版" Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The primary mechanism of copper-induced cell death. Activating stress pathways (endoplasmic reticulum stress and oxidative stress), blocking the cell cycle, and anti-angiogenesis are all used to treat cancer by controlling copper levels and utilizing the cytotoxicity produced by copper excess to kill tumor cells. There are other therapeutic mechanisms to treat cancer by reaching the tumor’s exact location in mice suffering from the tumor and causing tumor cell death under the action of copper.
Figure 2
Figure 2
Chemical structure of Cu1 (A) complex and Cu2 (B).
Figure 3
Figure 3
Copper-binding inhibitors induce reactive oxygen species production and deoxy ribosyl purine depletion. Treatment of cancer cells with copper in combination with NSC319726 enhances the inhibitory effect of this compound on cancer cells, leading to the intracellular production of reactive oxygen species and the depletion of deoxyribonucleopurines (e.g., 20-deoxyguanosine), inducing cellular G-phase arrest and apoptosis.
Figure 4
Figure 4
Chemical structure of disulfiram/copper complexes.
Figure 5
Figure 5
Chemical structure of [(H2L2)Cu(μ-Cl)2Cu(H2L2)]Cl2·5H2O, [(H2L2)Cu(μ-Cl)2Cu(H2L2)]Cl2·5H2O, [(HL1)Cu(μ-Cl)2Cu(HL1)]Cl2·H2O, [(HL3)Cu(μ-Cl)2Cu(HL3)]Cl2·4H2O.
Figure 6
Figure 6
Chemical structure of [Cu2L1–5(ClO4)](ClO4) (A), chemical structure of [Cu(L1)(phen)](ClO4) and [Cu(L2)(bpy)](ClO4) (B) and chemical structure of copper(II) tripyridine complex (C).
See this image and copyright information in PMC

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