Serum and Tissue Trace Metal Levels in Lung Cancer

Díez, Mercedes Díaz de Cerio; Arroyo, María Castellano; Cerdan, F; Muñoz, M. Lopez; Martin, Madeline; Jl, Balibrea

doi:10.1159/000226722

Cited by 143 publications

(112 citation statements)

References 3 publications

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“…A unique feature of cancer cells is to accumulate high concentrations of copper. It was previously reported that certain types of organiccopper complexes are capable of apoptosis induction that is not a result of oxidative effects [22]. Therefore, the capability of organic copper to induce apoptosis, the necessity of copper for angiogenesis, and the accumulation of copper by cancer cells and tissues allows for a novel therapeutic strategy focusing on elevated copper as a selection mechanism against cancer cells and tissues.…”

Section: Biochemical Determinationsmentioning

confidence: 99%

The Role of Novel 3d-Copper Cyanide Supramolecular Coordination Polymer in Epithelial Mesenchymal Transition Inhibition in Hepatocellular Carcinoma

Darwish¹,

Elshikh²,

Sultan³

et al. 2017

Biochem Pharmacol

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Section: Biochemical Determinationsmentioning

confidence: 99%

The Role of Novel 3d-Copper Cyanide Supramolecular Coordination Polymer in Epithelial Mesenchymal Transition Inhibition in Hepatocellular Carcinoma

Darwish¹,

Elshikh²,

Sultan³

et al. 2017

Biochem Pharmacol

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“…Having these important physiologic functions, it is not surprising that the concentrations of both zinc and copper are tightly regulated in an organism (Maverakis et al, 2007;Labbe and Thiele, 1999). Interestingly, disturbed zinc homeostasis and the elevated copper level have been reported in many types of cancer, including breast, prostate, lung, and brain (Geraki et al, 2002;Nayak et al, 2003;Diez et al, 1989;Yoshida et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Pyrrolidine dithiocarbamate-zinc(II) and -copper(II) complexes induce apoptosis in tumor cells by inhibiting the proteasomal activity

Milacic

Chen

Giovagnini

et al. 2008

Toxicology and Applied Pharmacology

143

128

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Zinc and copper are trace elements essential for proper folding, stabilization and catalytic activity of many metalloenzymes in living organisms. However, disturbed zinc and copper homeostasis is reported in many types of cancer. We have previously demonstrated that copper complexes induced proteasome inhibition and apoptosis in cultured human cancer cells. In the current study we hypothesized that zinc complexes could also inhibit the proteasomal chymotrypsin-like activity responsible for subsequent apoptosis induction. We first showed that zinc(II) chloride was able to inhibit the chymotrypsin-like activity of a purified 20S proteasome with an IC 50 value of 13.8 μM, which was less potent than copper(II) chloride (IC 50 5.3 μM). We then compared the potencies of a pyrrolidine dithiocarbamate (PyDT)-zinc(II) complex and a PyDT-copper(II) complex to inhibit cellular proteasomal activity, suppress proliferation and induce apoptosis in various human breast and prostate cancer cell lines. Consistently, zinc complex was less potent than copper complex in inhibiting the proteasome and inducing apoptosis. Additionally, zinc and copper complexes appear to use somewhat different mechanisms to kill tumor cells. Zinc complexes were able to activate calpain-, but not caspase-3-dependent pathway, while copper complexes were able to induce activation of both proteases. Furthermore, the potencies of these PyDT-metal complexes depend on the nature of metals and also on the ratio of PyDT to the metal ion within the complex, which probably affects their stability and availability for interacting with and inhibiting the proteasome in tumor cells.

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“…High serum and tissue levels of copper have been observed in a variety of human tumors including brain (21), breast (22)(23), colon (24), lung (25), and prostate (24,26). In 1980, it was first noticed that Cu played a critical role in angiogenesis (27).…”

Section: Coppermentioning

confidence: 99%

New applications of old metal-binding drugs in the treatment of human cancer

Dou¹

2012

Front Biosci

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Significant advances in the use of metal complexes, precipitated by platinum, have fostered a renewed interest in harnessing their rich potential in the treatment of cancer. In addition to platinum-based complexes, the anticancer properties of other metals such as ruthenium have been realized, and ruthenium-based compounds are currently being investigated in clinical trials. Since the process of drug development can be expensive and cumbersome, finding new applications of existing drugs may provide effective means to expedite the regulatory process in bringing new drugs to the clinical setting. Encouraging findings from laboratory studies reveal significant anticancer activity from different classes of metal-chelating compounds, such as disulfiram, clioquinol, and dithiocarbamate derivatives that are currently approved for the treatment of various pathological disorders. Their use as coordination complexes with metals such as copper, zinc, and gold that target the ubiquitin-proteasome pathway have shown significant promise as potential anticancer agents. This review discusses the unique role of several selected metals in relation to their anti-cancer properties as well as the new therapeutic potential of several previously approved metal-chelating drugs. In vitro and in vivo experimental evidence along with mechanisms of action (e.g., via targeting the tumor proteasome) will also be discussed with anticipation of strengthening this exciting new concept. KeywordsDisulfiram; Clioquinol; Dithiocarbamates; Copper; Zinc; Ubiquitin-Proteasome Pathway; Proteasome Inhibitor; Chymotrypsin-Like Activity; Review INTRODUCTION The use of metal complexes for cancer treatmentThe development of metal-based complexes for the treatment of cancer began with the discovery of the anti-cancer properties of cisplatin in the early 1960s (Figure 1). Over 90% of testicular cancer cases have been cured by cisplatin, and it has also been important in the treatment of several other types of cancer, including ovarian, cervical, bladder, head and neck, melanoma, and lymphomas (1). Cisplatin interacts with DNA and forms adducts which interfere with the replication and transcription processes, and ultimately triggers apoptosis (2). These cisplatin-DNA interactions have been extensively studied, and it has been clearly shown that a (Pt)-GG intrastrand cross-link is responsible for the cytotoxicity of Send correspondence to: Qing Ping Dou, The Developmental Therapeutics Program, Barbara Ann Karmanos Cancer Institute, and Departments of Oncology, Pharmacology and Pathology, School of Medicine, Wayne State University, Detroit, Michigan 48201, USA, doup@karmanos.org. NIH Public Access Author ManuscriptFront Biosci (Schol Ed). Author manuscript; available in PMC 2013 May 07. Published in final edited form as:Front Biosci (Schol Ed). ; 4: 375-391. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript cisplatin (3). However, the toxicities associated with cisplatin, coupled with intrinsic and acquired drug resistance, ha...

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Serum and Tissue Trace Metal Levels in Lung Cancer

Cited by 143 publications

References 3 publications

The Role of Novel 3d-Copper Cyanide Supramolecular Coordination Polymer in Epithelial Mesenchymal Transition Inhibition in Hepatocellular Carcinoma

The Role of Novel 3d-Copper Cyanide Supramolecular Coordination Polymer in Epithelial Mesenchymal Transition Inhibition in Hepatocellular Carcinoma

Pyrrolidine dithiocarbamate-zinc(II) and -copper(II) complexes induce apoptosis in tumor cells by inhibiting the proteasomal activity

New applications of old metal-binding drugs in the treatment of human cancer

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