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Review
. 2024 Jun 21;25(13):6842.
doi: 10.3390/ijms25136842.

Assessment of the Impact of Trace Essential Metals on Cancer Development

Affiliations
Review

Assessment of the Impact of Trace Essential Metals on Cancer Development

Aleksandra Górska et al. Int J Mol Sci. .

Abstract

This study examines the impact of zinc, copper, cobalt, iron, and manganese on cancer development, considering their dual roles as potential promoters or inhibitors within tumorigenesis. A comprehensive analysis of existing literature and experimental data is conducted to elucidate the intricate relationship between these trace elements and cancer progression. The findings highlight the multifaceted effects of zinc, copper, cobalt, iron, and manganese on various aspects of cancer development, including cell proliferation, angiogenesis, and metastasis. Understanding the nuanced interactions between these trace elements and cancer could offer crucial insights into tumorigenesis mechanisms and facilitate the identification of novel biomarkers and therapeutic targets for cancer prevention and treatment strategies. This research underscores the importance of considering the roles of essential trace elements in cancer biology and may ultimately contribute to advancements in precision medicine approaches for combating cancer.

Keywords: carcinogenesis; cobalt; copper; heavy metals; iron; manganese; zinc.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The anticarcinogenic effect of zinc. ROS, reactive oxygen species. RNS, reactive nitrogen species [14,15].
Figure 2
Figure 2
Copper’s carcinogenic potential. IL-17, interleukin 17. Cu+, Cu2+, copper ions. CTR1, high-affinity copper uptake protein 1 (copper transporter 1). MAP kinase pathway, mitogen-activated protein kinase pathway. MEK1, mitogen-activated proteinkinase kinase 1. ERK1/2, extracellular signal-regulated kinases 1 and 2. PI3K, phosphoinositide 3-kinase. ATK, agammaglobulinemia tyrosine kinase. FoxO1a, forehead box O1a. ROS, reactive oxygen species. XIAP, X-linked inhibitor of apoptosis. NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells. E3 ligase, E3 ubiquitin ligase [25,27,32,35,36,37,38,39,43,44,45].
Figure 3
Figure 3
The relationship between cobalt and carcinogenesis. The cobalt atom can interact with DNA, and processes such as oxidative stress and DNA damage are the main mechanisms by which cobalt can induce carcinogenesis. Exposure to cobalt leads to changes in DNA which can result in the development of cancer [54,55].
Figure 4
Figure 4
Link between manganese and carcinogenesis. The figure shows how exposure to manganese can lead to DNA damage, which in turn can trigger carcinogenic processes, leading to the development of cancer [92,94].

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