Quantitative Analyses of ROS and RNS Production in Breast Cancer Cell Lines Incubated with Ferrocifens

Lu, Cong; Heldt, Jan‐Martin; Guille‐Collignon, Manon; Lemaître, Frédéric; Jaouen, Gérard; Vessières, Anne; Amatore, Christian

doi:10.1002/cmdc.201402016

Cited by 47 publications

(57 citation statements)

References 35 publications

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“…As far as production of ROS by Jurkat cells is concerned, complex 2 induces greater production than 1, which was also observed in the ferrocifen series [40]. This ROS production would be the source of the increase in activity of glutathione reductase.…”

Section: Methodsmentioning

confidence: 73%

Osmocenyl-tamoxifen derivatives target the thioredoxin system leading to a redox imbalance in Jurkat cells

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Lee

et al. 2016

Journal of Inorganic Biochemistry

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ABSTRACT:To complete our study of the iron, ruthenium and osmium metallocene triad derived from hydroxytamoxifen, we report here the synthesis and study of the biological effects of two ferrocifen analogs in the osmium series, namely the monophenolic complex 1, the tamoxifen- within the cell and that inhibition of thioredoxin reductase is a key factor in rationalizing the cytotoxicity of these complexes on Jurkat cells.

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Section: Methodsmentioning

confidence: 73%

Osmocenyl-tamoxifen derivatives target the thioredoxin system leading to a redox imbalance in Jurkat cells

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Lee

et al. 2016

Journal of Inorganic Biochemistry

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“…The results corroborate our assertion that both catecholamines and glucocorticoids, at physiological levels, can increase DNA damage through receptor-mediated signalling. The use of electrochemical analyses to quantify production of ROS/RNS in response to ferrocifens in breast cancer has also been explored previously [28], indicating that TNBC cells produce ROS/RNS in response to stimuli.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids induce production of reactive oxygen species/reactive nitrogen species and DNA damage through an iNOS mediated pathway in breast cancer

et al. 2017

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BackgroundPsychological stress increases the circulating levels of the stress hormones cortisol and norepinephrine (NE). Chronic exposure to elevated stress hormones has been linked to a reduced response to chemotherapy through induction of DNA damage. We hypothesize that stress hormone signalling may induce DNA damage through the production of reactive oxygen species (ROS)/reactive nitrogen species (RNS) and interference in DNA repair processes, promoting tumourigenesis.MethodsBreast cancer cell lines were incubated with physiological levels of cortisol and NE in the presence and absence of receptor antagonists and inducible nitric oxide synthase (iNOS) inhibitors and DNA damage measured using phosphorylated γ-H2AX. The rate of DNA repair was measured using comet assays and electrochemical sensors were used to detect ROS/RNS in the cell lysates from cells exposed to stress hormones. A syngeneic mouse model was used to assess the presence of iNOS in mammary tumours in stressed versus control animals and expression of iNOS was examined using western blotting and qRT-PCR.ResultsAcute exposure to cortisol and NE significantly increased levels of ROS/RNS and DNA damage and this effect was diminished in the presence of receptor antagonists. Cortisol induced DNA damage and the production of RNS was further attenuated in the presence of an iNOS inhibitor. An increase in the expression of iNOS in response to psychological stress was observed in vivo and in cortisol-treated cells. Inhibition of glucocorticoid receptor-associated Src kinase also produced a decrease in cortisol-induced RNS.ConclusionThese results demonstrate that glucocorticoids may interact with iNOS in a non-genomic manner to produce damaging levels of RNS, thus allowing an insight into the potential mechanisms by which psychological stress may impact breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-017-0823-8) contains supplementary material, which is available to authorized users.

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“…Mechanistic studies of ferrocifens highlighted cytostatic properties on tumors, thus causing death of cells by senescence. The presence of side‐chain amino groups on ferrocifen complexes leads to major toxicity, similar to the one observed with other metallocenes . Extending the promising results using metallocenes, half sandwich iron(II) cyclopentadienyl complexes (e.g.…”

Section: Introductionmentioning

confidence: 63%

“…One area that has certainly received a significant attention is the application of coordination and organometallic complexes as drugs or prodrugs in the cancer treatment . The readily available and inexpensive iron is a good candidate as a key component in many important biological processes, and ferrocene derivatives are among the most studied iron complexes for their bio‐inorganic properties related to their reactivity and electrochemical properties . Mechanistic studies of ferrocifens highlighted cytostatic properties on tumors, thus causing death of cells by senescence.…”

Section: Introductionmentioning

confidence: 99%

Synthesis, reactivity and preliminary biological activity of iron(0) complexes with cyclopentadienone and amino‐appended N‐heterocyclic carbene ligands

Cingolani

Zanotti

Zacchini

et al. 2019

Applied Organom Chemis

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Neutral and cationic cyclopentadienone (CpO) N‐heterocyclic carbene (NHC) bis‐carbonyl iron(0) complexes bearing, appended to the NHC ligand, either a terminal amino group on the lateral chain, [Fe(η4‐CpO)(CO)2(κC‐NHC(CH2)nNH2)] with n = 2 (2a) and 3 (2b), or a cationic NMe3+ fragment, [Fe(η4‐CpO)(CO)2(κC‐NHC(CH2)2NMe3)](I) (3), were prepared and characterized in terms of their structure, stability and reactivity. The photochemical properties of 2a and 2b were examined both in organic solvents and in water, revealing the photoactivated release of one CO ligand followed by the formation of the chelated complex [Fe(η4‐CpO)(CO)(κ2C,N‐NHC(CH2)2NH2)] (4), whose molecular structure was confirmed by single crystal X‐ray diffraction studies. This metallacyclization occurs only in the case of 2a, with the ethylene spacer between NHC ring and NH2 group in the lateral chain, allowing the formation of a stable 6‐membered ring. On the other hand, 2b undergoes decomposition upon irradiation. The reactivity in aqueous solutions revealed the chemical speciation of the complexes at different pH and especially under physiological conditions (phosphate buffer solution at pH 7.4 and 37 °C). The lack of data on the biological properties of iron(0) complexes prompted us to preliminarily investigate their cytotoxicity against model cancer cells (AsPC‐1 and HPAF‐II), along with a determination of their lipophilicity.

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Quantitative Analyses of ROS and RNS Production in Breast Cancer Cell Lines Incubated with Ferrocifens

Cited by 47 publications

References 35 publications

Osmocenyl-tamoxifen derivatives target the thioredoxin system leading to a redox imbalance in Jurkat cells

Osmocenyl-tamoxifen derivatives target the thioredoxin system leading to a redox imbalance in Jurkat cells

Glucocorticoids induce production of reactive oxygen species/reactive nitrogen species and DNA damage through an iNOS mediated pathway in breast cancer

Synthesis, reactivity and preliminary biological activity of iron(0) complexes with cyclopentadienone and amino‐appended N‐heterocyclic carbene ligands

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