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Article: The Chemical Biology of NO that Regulates Oncogenic Signaling and Metabolism: NOS2 and Its Role in Inflammatory Disease.

Miranda, Katrina M / Ridnour, Lisa A / Cheng, Robert Y S / Wink, David A / Thomas, Douglas D

2023 Volume 28, Issue 1, Page(s) 27–45

Abstract: Nitric oxide (NO) and the enzyme that synthesizes it, nitric oxide synthase 2 (NOS2), have emerged as key players in inflammation and cancer. Expression of NOS2 in tumors has been correlated both with positive outcomes and with poor prognoses. The ... ...

Abstract	Nitric oxide (NO) and the enzyme that synthesizes it, nitric oxide synthase 2 (NOS2), have emerged as key players in inflammation and cancer. Expression of NOS2 in tumors has been correlated both with positive outcomes and with poor prognoses. The chemistry of NO is the major determinate to the biological outcome and the concentration of NO, which can range over five orders of magnitude, is critical in determining which pathways are activated. It is the activation of specific oncogenic and immunological mechanisms that shape the outcome. The kinetics of specific reactions determine the mechanisms of action. In this review, the relevant reactions of NO and related species are discussed with respect to these oncogenic and immunological signals.
MeSH term(s)	Humans ; Neoplasms/genetics ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Signal Transduction
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; NOS2 protein, human (EC 1.14.13.39)
Language	English
Publishing date	2023-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036388-9
ISSN	0893-9675
ISSN	0893-9675
DOI	10.1615/CritRevOncog.2023047302
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Article ; Online: Chronic Exposure to Nitric Oxide Induces P53 Mutations and Malignant-like Features in Human Breast Epithelial Cells.

Cheng, Robert Y S / Burkett, Sandra / Ambs, Stefan / Moody, Terry / Wink, David A / Ridnour, Lisa A

Biomolecules

2023 Volume 13, Issue 2

Abstract: The small endogenous signaling molecule nitric oxide (NO) has been linked with chronic inflammation and cancer. The effects of NO are both concentration and temporally dependent; under some conditions, NO protects against damage caused by reactive oxygen ...

Abstract	The small endogenous signaling molecule nitric oxide (NO) has been linked with chronic inflammation and cancer. The effects of NO are both concentration and temporally dependent; under some conditions, NO protects against damage caused by reactive oxygen species and activates P53 signaling. During chronic inflammation, NO causes DNA damage and inhibits repair proteins. To extend our understanding of the roles of NO during carcinogenesis, we investigated the possible effects of chronic NO exposure on MCF10A breast epithelial cells, as defined by changes in cellular morphology, chromosome/genomic stability, RNA, and protein expression, and altered cell phenotypes. Human MCF10A cells were maintained in varying doses of the NO donor DETANO for three weeks. Distinct patterns of genomic modifications in TP53 and KRAS target genes were detected in NO-treated cells when compared to background mutations. In addition, quantitative real-time PCR demonstrated an increase in the expression of cancer stem cell (CSC) marker CD44 after prolonged exposure to 300 μM DETANO. While similar changes in cell morphology were found in cells exposed to 300-500 μM DETANO, cells cultured in 100 μM DETANO exhibited enhanced motility. In addition, 100 μM NO-treated cells proliferated in serum-free media and selected clonal populations and pooled cells formed colonies in soft agar that were clustered and disorganized. These findings show that chronic exposure to NO generates altered breast epithelial cell phenotypes with malignant characteristics.
MeSH term(s)	Humans ; Female ; Nitric Oxide/metabolism ; Tumor Suppressor Protein p53/metabolism ; Epithelial Cells/metabolism ; Mutation ; Inflammation/metabolism ; Breast Neoplasms/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-02-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13020311
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Article ; Online: Nitric Oxide and Cancer: When to Give and When to Take Away?

Miranda, Katrina M / Ridnour, Lisa A / McGinity, Christopher L / Bhattacharyya, Dana / Wink, David A

Inorganic chemistry

2021 Volume 60, Issue 21, Page(s) 15941–15947

Abstract: The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, ... ...

Abstract	The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment. In this Viewpoint, the current understanding of the concentration, spatial, and temporal dependence of responses to NO is correlated with potential treatment and prevention technologies and strategies.
MeSH term(s)	Nitric Oxide
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2021-10-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1484438-2
ISSN	1520-510X ; 0020-1669
ISSN (online)	1520-510X
ISSN	0020-1669
DOI	10.1021/acs.inorgchem.1c02434
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Article: HNO Protects the Myocardium against Reperfusion Injury, Inhibiting the mPTP Opening via PKCε Activation.

Mancardi, Daniele / Pagliaro, Pasquale / Ridnour, Lisa A / Tocchetti, Carlo G / Miranda, Katrina / Juhaszova, Magdalena / Sollott, Steven J / Wink, David A / Paolocci, Nazareno

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 2

Abstract: Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide ( ... ...

Abstract	Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO
Language	English
Publishing date	2022-02-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11020382
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Article: HNO Protects the Myocardium against Reperfusion Injury, Inhibiting the mPTP Opening via PKC Activation

Mancardi, Daniele / Pagliaro, Pasquale / Ridnour, Lisa A. / Tocchetti, Carlo G. / Miranda, Katrina / Juhaszova, Magdalena / Sollott, Steven J. / Wink, David A. / Paolocci, Nazareno

Antioxidants. 2022 Feb. 14, v. 11, no. 2

2022

Abstract: Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO.), positively modulate cardiac contractility/relaxation while limiting ischemia-reperfusion (I/R) injury. The mechanisms underpinning HNO anti-ischemic effects remain poorly ...

Abstract	Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO.), positively modulate cardiac contractility/relaxation while limiting ischemia-reperfusion (I/R) injury. The mechanisms underpinning HNO anti-ischemic effects remain poorly understood. Using isolated perfused rat hearts subjected to 30 min global ischemia/1 or 2 h reperfusion, here we tested whether, in analogy to NO., HNO protection requires PKC translocation to mitochondria and KATP channels activation. To this end, we compared the benefits afforded by ischemic preconditioning (IPC; 3 cycles of I/R) with those eventually granted by the NO. donor, diethylamine/NO, DEA/NO, and two chemically unrelated HNO donors: Angeli’s salt (AS, a prototypic donor) and isopropylamine/NO (IPA/NO, a new HNO releaser). All donors were given for 19 min before I/R injury. In control I/R hearts (1 h reperfusion), infarct size (IS) measured via tetrazolium salt staining was 66 ± 5.5% of the area at risk. Both AS and IPA/NO were as effective as IPC in reducing IS [30.7 ± 2.2 (AS), 31 ± 2.9 (IPA/NO), and 31 ± 0.8 (IPC), respectively)], whereas DEA/NO was significantly less so (36.2 ± 2.6%, p < 0.001 vs. AS, IPA/NO, or IPC). IPA/NO protection was still present after 120 min of reperfusion, and the co-infusion with the PKC inhibitor (PKCV1-2500 nM) prevented it (IS = 30 ± 0.5 vs. 61 ± 1.8% with IPA/NO alone, p < 0.01). Irrespective of the donor, HNO anti-ischemic effects were insensitive to the KATP channel inhibitor, 5-OH decanoate (5HD, 100 μM), that, in contrast, abrogated DEA/NO protection. Finally, both HNO donors markedly enhanced the mitochondrial permeability transition pore (mPTP) ROS threshold over control levels (≅35–40%), an action again insensitive to 5HD. Our study shows that HNO donors inhibit mPTP opening, thus limiting myocyte loss at reperfusion, a beneficial effect that requires PKC translocation to the mitochondria but not mitochondrial K⁺ channels activation.
Keywords	infarction ; mitochondria ; myocardium ; nitric oxide ; permeability ; rats ; reperfusion injury ; risk ; tetrazolium
Language	English
Dates of publication	2022-0214
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11020382
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: New nitrosyl ruthenium complexes with combined activities for multiple cardiovascular disorders.

Gouveia Júnior, Florêncio Sousa / Silveira, João Alison de Moraes / Holanda, Thais Muratori / Marinho, Aline Diogo / Ridnour, Lisa A / Wink, David A / de Siqueira, Rodrigo José Bezerra / Monteiro, Helena Serra Azul / Sousa, Eduardo Henrique Silva de / Lopes, Luiz Gonzaga de França

Dalton transactions (Cambridge, England : 2003)

2023 Volume 52, Issue 16, Page(s) 5176–5191

Abstract: Nitrosyl ruthenium complexes are promising platforms for nitric oxide (NO) and nitroxyl (HNO) release, which exert their therapeutic application. In this context, we developed two polypyridinic compounds with the general ... ...

Abstract	Nitrosyl ruthenium complexes are promising platforms for nitric oxide (NO) and nitroxyl (HNO) release, which exert their therapeutic application. In this context, we developed two polypyridinic compounds with the general formula
MeSH term(s)	Animals ; Rats ; Coordination Complexes ; Nitric Oxide/chemistry ; Nitrogen Oxides/chemistry ; Ruthenium/chemistry ; Sulfhydryl Compounds/chemistry ; Cardiovascular Diseases
Chemical Substances	Coordination Complexes ; Nitric Oxide (31C4KY9ESH) ; Nitrogen Oxides ; nitroxyl (GFQ4MMS07W) ; Ruthenium (7UI0TKC3U5) ; Sulfhydryl Compounds
Language	English
Publishing date	2023-04-25
Publishing country	England
Document type	Journal Article
ZDB-ID	1472887-4
ISSN	1477-9234 ; 1364-5447 ; 0300-9246 ; 1477-9226
ISSN (online)	1477-9234 ; 1364-5447
ISSN	0300-9246 ; 1477-9226
DOI	10.1039/d3dt00059a
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model.

Cheng, Robert Y S / Patel, Nimit L / Back, Timothy / Basudhar, Debashree / Somasundaram, Veena / Kalen, Joseph D / Wink, David A / Ridnour, Lisa A

Journal of visualized experiments : JoVE

2020 , Issue 157

Abstract: Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited therapeutic options. When compared to patients with less aggressive breast tumors, the 5-year survival rate of TNBC patients is 77% due to their characteristic drug- ... ...

Abstract	Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited therapeutic options. When compared to patients with less aggressive breast tumors, the 5-year survival rate of TNBC patients is 77% due to their characteristic drug-resistant phenotype and metastatic burden. Toward this end, murine models have been established aimed at identifying novel therapeutic strategies limiting TNBC tumor growth and metastatic spread. This work describes a practical guide for the TNBC orthotopic model where MDA-MB-231 breast cancer cells suspended in a basement membrane matrix are implanted in the fourth mammary fat pad, which closely mimics the cancer cell behavior in humans. Measurement of tumors by caliper, lung metastasis assessment via in vivo and ex vivo imaging, and molecular detection are discussed. This model provides an excellent platform to study therapeutic efficacy and is especially suitable for the study of the interaction between the primary tumor and distal metastatic sites.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Female ; Humans ; Lung Neoplasms/secondary ; Mice ; Phenotype ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/60316
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Studying triple negative breast cancer using orthotopic breast cancer model

Cheng, Robert Y. S / Patel, Nimit L / Back, Timothy / Basudhar, Debashree / Somasundaram, Veena / Kalen, Joseph D / Wink, David A / Ridnour, Lisa A

Journal of visualized experiments. 2020 Mar. 20, , no. 157

2020

Abstract	Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited therapeutic options. When compared to patients with less aggressive breast tumors, the 5-year survival rate of TNBC patients is 77% due to their characteristic drug-resistant phenotype and metastatic burden. Toward this end, murine models have been established aimed at identifying novel therapeutic strategies limiting TNBC tumor growth and metastatic spread. This work describes a practical guide for the TNBC orthotopic model where MDA-MB-231 breast cancer cells suspended in a basement membrane matrix are implanted in the fourth mammary fat pad, which closely mimics the cancer cell behavior in humans. Measurement of tumors by caliper, lung metastasis assessment via in vivo and ex vivo imaging, and molecular detection are discussed. This model provides an excellent platform to study therapeutic efficacy and is especially suitable for the study of the interaction between the primary tumor and distal metastatic sites.
Keywords	animal models ; basement membrane ; breast neoplasms ; drug resistance ; humans ; image analysis ; lungs ; metastasis ; neoplasm cells ; patients ; phenotype ; survival rate ; therapeutics
Language	English
Dates of publication	2020-0320
Size	p. e60316.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/60316
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Nitric Oxide Modulates Metabolic Processes in the Tumor Immune Microenvironment.

McGinity, Christopher L / Palmieri, Erika M / Somasundaram, Veena / Bhattacharyya, Dibyangana D / Ridnour, Lisa A / Cheng, Robert Y S / Ryan, Aideen E / Glynn, Sharon A / Thomas, Douglas D / Miranda, Katrina M / Anderson, Stephen K / Lockett, Stephen J / McVicar, Daniel W / Wink, David A

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: The metabolic requirements and functions of cancer and normal tissues are vastly different. Due to the rapid growth of cancer cells in the tumor microenvironment, distorted vasculature is commonly observed, which creates harsh environments that require ... ...

Abstract	The metabolic requirements and functions of cancer and normal tissues are vastly different. Due to the rapid growth of cancer cells in the tumor microenvironment, distorted vasculature is commonly observed, which creates harsh environments that require rigorous and constantly evolving cellular adaption. A common hallmark of aggressive and therapeutically resistant tumors is hypoxia and hypoxia-induced stress markers. However, recent studies have identified alterations in a wide spectrum of metabolic pathways that dictate tumor behavior and response to therapy. Accordingly, it is becoming clear that metabolic processes are not uniform throughout the tumor microenvironment. Metabolic processes differ and are cell type specific where various factors promote metabolic heterogeneity within the tumor microenvironment. Furthermore, within the tumor, these metabolically distinct cell types can organize to form cellular neighborhoods that serve to establish a pro-tumor milieu in which distant and spatially distinct cellular neighborhoods can communicate via signaling metabolites from stroma, immune and tumor cells. In this review, we will discuss how biochemical interactions of various metabolic pathways influence cancer and immune microenvironments, as well as associated mechanisms that lead to good or poor clinical outcomes.
MeSH term(s)	Animals ; Humans ; Neoplasms/immunology ; Neoplasms/pathology ; Nitric Oxide/immunology ; Signal Transduction/immunology ; Tumor Microenvironment/immunology
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2021-06-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22137068
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Article ; Online: The Oncogenic Properties Of The Redox Inflammatory Protein Inducible Nitric Oxide Synthase In ER(-) Breast Cancer.

Wink, David A / Ridnour, Lisa A / Cheng, Robert / Switzer, Christopher W / Glynn, Sharon / Ambs, Stefan

Redox biology

2015 Volume 5, Page(s) 413

Abstract: Inflammation generates reactive chemical species that induce conditions of oxidative nitrosative stress as emerged as factor in poor outcome of many cancers. Our recent findings show that in the inflammatory protein inducible nitric oxide synthase (iNOS) ...

Abstract	Inflammation generates reactive chemical species that induce conditions of oxidative nitrosative stress as emerged as factor in poor outcome of many cancers. Our recent findings show that in the inflammatory protein inducible nitric oxide synthase (iNOS) is a strong predictor of poor outcome in ER(-) patients (Glynn et al. JCI 2010). Furthermore 46 genes, of which 23 were associated with basal like breast cancer, were elevated when iNOS high. In vitro studies using ER(-) cell lines showed that fluxes of nitric oxide (NO) delivered by NO donors surprising mimic this relationship in the patient cohort. Using this model, we show that NO at different specific concentrations stimulate pro-oncogenic mechanisms such as AKT, ERK, NFkB, AP-1, and HIF-1α that lead to increase of metastatic and cancer stem cells proteins. In addition, we show that tumor suppressor gene BRCA1 and PP2A are inhibited by these NO levels. Similarly other studies show that these concentrations of NO increase immunosuppressive proteins TGF-β and IL-10 in leukocytes to decrease efficacy of some anticancer therapies further contributing to pro-tumorigenic environment. Using this model we have identified several new compounds that have efficacy in xenographic models. These finding have provided a model that shows how NO can affect numerous mechanism that leads to a more aggressive phenotype.
Language	English
Publishing date	2015-08
Publishing country	Netherlands
Document type	Journal Article
ISSN	2213-2317
ISSN (online)	2213-2317
DOI	10.1016/j.redox.2015.09.012
Database	MEDical Literature Analysis and Retrieval System OnLINE

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