Synthesis, biological characterization and evaluation of molecular mechanisms of novel copper complexes as anticancer agents

Acılan, Ceyda; Cevatemre, Buse; Adiguzel, Zelal; Karakaş, Didem; Ulukaya, Engin; Ribeiro, Nádia; Correia, Isabel; Pessoa, João Costa

doi:10.1016/j.bbagen.2016.10.014

Cited by 79 publications

(26 citation statements)

References 47 publications

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“…24,25 Previous studies indicate that copper(II) compounds can cause ROS/RNS to generate mitochondrial dysfunction and oxidative DNA damage, which ultimately results in the activation of the mitochondrial apoptosis pathway among cancer cells. 26,27 In summary, our results are in agreement with those reported for several copper and ruthenium compounds, whose attractive anticancer activity is related to their ability to generate ROS/RNS in cancer cells.…”

Section: Electrochemical Propertiessupporting

confidence: 91%

Cytotoxic effect, generation of reactive oxygen/nitrogen species and electrochemical properties of Cu(ii) complexes in comparison to half-sandwich complexes of Ru(ii) with aminochromone derivatives

et al. 2019

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Section: Electrochemical Propertiessupporting

confidence: 91%

Cytotoxic effect, generation of reactive oxygen/nitrogen species and electrochemical properties of Cu(ii) complexes in comparison to half-sandwich complexes of Ru(ii) with aminochromone derivatives

et al. 2019

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“…[2,3,9,[76][77][78] Although slowo xidation of V IV to V V speciesi n polar organic solvents and dissociation of the O,N,O-donor ligands in aqueousb uffer solutionsh ave been mentioned, [76][77][78] reactivity studies in biological media are lacking. Such studies are much needed to determine whether their activities are due to free ligands( or their Cu II complexes formed in biological media), [51,73,83] Vs pecies,o rb oth (Section3).…”

Section: Complexeswith On-donor Ligandsmentioning

confidence: 99%

Stabilities and Biological Activities of Vanadium Drugs: What is the Nature of the Active Species?

Levina

Lay

2017

Chemistry An Asian Journal

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Diverse biological activities of vanadium(V) drugs mainly arise from their abilities to inhibit phosphatase enzymes and to alter cell signaling. Initial interest focused on anti-diabetic activities but has shifted to anti-cancer and anti-parasitic drugs. V-based anti-diabetics are pro-drugs that release active components (e.g., H VO ) in biological media. By contrast, V anti-cancer drugs are generally assumed to enter cells intact; however, speciation studies indicate that nearly all drugs are likely to react in cell culture media during in vitro assays and the same would apply in vivo. The biological activities are due to V and/or V reaction products with cell culture media, or the release of ligands (e.g., aromatic diimines, 8-hydroxyquinolines or thiosemicarbazones) that bind to essential metal ions in the media. Careful consideration of the stability and speciation of V complexes in cell culture media and in biological fluids is essential to design targeted V-based anti-cancer therapies.

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“…Copper, as the active centre of many enzymes, plays an important role in development and function of human organs and tissues [20][21][22]. To date, copper-based complexes have been extensively synthesised and investigated as anticancer agents because of their high antitumor activity and advantages relative to other metal anticancer complexes [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38]. Thiosemicarbazones are formed by a condensation reaction of thiosemicarbazide and aldehydes or ketones.…”

Section: Introductionmentioning

confidence: 99%

Designing anticancer copper(II) complexes by optimizing 2-pyridine-thiosemicarbazone ligands

Deng

Zhang

et al. 2018

European Journal of Medicinal Chemistry

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To develop potential next-generation metal anticancer agents, we designed and synthesised five Cu(II) 2-pyridine-thiosemicarbazone complexes by modifying the hydrogen atom at the N-4 position of ligands, and then investigated their structure-activity relationships and anticancer mechanisms. Modification of the N-4 position with different groups caused significant differences in cellular uptake and produced superior antitumor activity. Cu complexes arrested the cell cycle at S phase, leading to down-regulation of levels of cyclin and cyclin-dependent kinases and up-regulation of expression of cyclin-dependent kinase inhibitors. Cu complexes exerted chemotherapeutic effects via activating p53 and inducing production of reactive oxygen species to regulate expression of the B-cell lymphoma-2 family of proteins, causing a change in the mitochondrial membrane potential and release of cytochrome c to form a dimer with apoptosis protease activating factor-1, resulting in activation of caspase-9/3 to induce apoptosis. In addition, Cu complexes inhibited telomerase by down-regulating the c-myc regulator gene and expression of the human telomerase reverse transcriptase.

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Synthesis, biological characterization and evaluation of molecular mechanisms of novel copper complexes as anticancer agents

Cited by 79 publications

References 47 publications

Cytotoxic effect, generation of reactive oxygen/nitrogen species and electrochemical properties of Cu(ii) complexes in comparison to half-sandwich complexes of Ru(ii) with aminochromone derivatives

Cytotoxic effect, generation of reactive oxygen/nitrogen species and electrochemical properties of Cu(ii) complexes in comparison to half-sandwich complexes of Ru(ii) with aminochromone derivatives

Stabilities and Biological Activities of Vanadium Drugs: What is the Nature of the Active Species?

Designing anticancer copper(II) complexes by optimizing 2-pyridine-thiosemicarbazone ligands

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