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Article ; Online: Methods to the madness - Fundamental techniques in NO research.

Thomas, Douglas D / Shiva, Sruti

2022 Volume 122-123, Page(s) 45–46

Language	English
Publishing date	2022-03-09
Publishing country	United States
Document type	Editorial
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2022.03.003
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Article ; Online: Breathing new life into nitric oxide signaling: A brief overview of the interplay between oxygen and nitric oxide.

Thomas, Douglas D

Redox biology

2015 Volume 5, Page(s) 225–233

Abstract: Nitric oxide ((•)NO, nitrogen monoxide) is one of the most unique biological signaling molecules associated with a multitude of physiologic and pathological conditions. In order to fully appreciate its numerous roles, it is essential to understand its ... ...

Abstract	Nitric oxide ((•)NO, nitrogen monoxide) is one of the most unique biological signaling molecules associated with a multitude of physiologic and pathological conditions. In order to fully appreciate its numerous roles, it is essential to understand its basic biochemical properties. Most signaling effector molecules such as steroids or proteins have a significant life-span and function through classical receptor-ligand interactions. (•)NO, however, is a short-lived free-radical gas that only reacts with two types of molecules under biological conditions; metals and other free radicals. These simple interactions can lead to a myriad of complex intermediates which in turn have their own phenotypic effects. For these reasons, responses to (•)NO often appear to be random or contradictory when outcomes are compared across various experimental settings. This article will serve as a brief overview of the chemical, biological, and microenvironmental factors that dictate (•)NO signaling with an emphasis on (•)NO metabolism. The prominent role that oxygen (dioxygen, O2) plays in (•)NO metabolism and how it influences the biological effects of (•)NO will be highlighted. This information and these concepts are intended to help students and investigators think about the interpretation of data from experiments where biological effects of (•)NO are being elucidated.
MeSH term(s)	Animals ; Free Radicals/chemistry ; Free Radicals/metabolism ; Half-Life ; Iron/chemistry ; Nitric Oxide/chemistry ; Nitric Oxide/metabolism ; Oxygen/chemistry ; Oxygen/metabolism ; Signal Transduction
Chemical Substances	Free Radicals ; Nitric Oxide (31C4KY9ESH) ; Iron (E1UOL152H7) ; Oxygen (S88TT14065)
Language	English
Publishing date	2015-05-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	2213-2317
ISSN (online)	2213-2317
DOI	10.1016/j.redox.2015.05.002
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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

Critical reviews in oncogenesis

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: Nitric oxide and hydrogen sulfide: Sibling rivalry in the family of epigenetic regulators.

Kuschman, Hannah Petraitis / Palczewski, Marianne B / Thomas, Douglas D

Free radical biology & medicine

2021 Volume 170, Page(s) 34–43

Abstract: Nitric oxide (NO) and hydrogen sulfide ( ... ...

Abstract	Nitric oxide (NO) and hydrogen sulfide (H
MeSH term(s)	Epigenesis, Genetic ; Gasotransmitters/metabolism ; Humans ; Hydrogen Sulfide/metabolism ; Nitric Oxide/metabolism ; Siblings
Chemical Substances	Gasotransmitters ; Nitric Oxide (31C4KY9ESH) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2021.01.010
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Article ; Online: NOS2 as an Emergent Player in Progression of Cancer.

Thomas, Douglas D / Wink, David A

Antioxidants & redox signaling

2017 Volume 26, Issue 17, Page(s) 963–965

Abstract: Although the inducible form of nitric oxide synthase (NOS2) was initially shown to be a major player as an antitumor component of the immune response, more recent data have shown that NOS2 expression in cancer cells often predicts poor outcome. Unlike ... ...

Abstract	Although the inducible form of nitric oxide synthase (NOS2) was initially shown to be a major player as an antitumor component of the immune response, more recent data have shown that NOS2 expression in cancer cells often predicts poor outcome. Unlike growth factors associated with a single oncogenic pathway, nitric oxide (NO) has a ubiquitous nature wherein it simultaneously mediates major oncogenic pathways from Akt/PI3K and RAS/ERK to HIF1a and TGFb. These interactive loops perpetuate oncogenic mechanism that leads to increased cancer stemness, proliferation metastasis, chemoresistance, angiogenesis, and immunosuppression. Examination of a wide variety of patient tumors demonstrates that NOS2 expression is >50% for most cancers. In many cases, elevated NOS2 has been shown to predict poor outcome in cancer such as ER- breast cancer, glioma, melanoma, cervical, liver, ovarian, and pancreatic. Taken together, NOS2 may be one of the most powerful biomarker and predictors of poor prognosis and an ideal target for cancer therapy. Antioxid. Redox Signal. 26, 963-965.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Neoplasm Metastasis ; Neoplasms/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Prognosis ; Signal Transduction ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; Nitric Oxide (31C4KY9ESH) ; NOS2 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2017--10
Publishing country	United States
Document type	Editorial ; Introductory Journal Article
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2016.6835
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Zs.A 5488: Show issues

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Article ; Online: Vorinostat exhibits anticancer effects in triple-negative breast cancer cells by preventing nitric oxide-driven histone deacetylation.

Palczewski, Marianne B / Kuschman, Hannah Petraitis / Bovee, Rhea / Hickok, Jason R / Thomas, Douglas D

Biological chemistry

2021 Volume 402, Issue 4, Page(s) 501–512

Abstract: Triple-negative breast cancers (TNBC) that produce nitric oxide (NO) are more aggressive, and the expression of the inducible form of nitric oxide synthase (NOS2) is a negative prognostic indicator. In these studies, we set out to investigate potential ... ...

Abstract	Triple-negative breast cancers (TNBC) that produce nitric oxide (NO) are more aggressive, and the expression of the inducible form of nitric oxide synthase (NOS2) is a negative prognostic indicator. In these studies, we set out to investigate potential therapeutic strategies to counter the tumor-permissive properties of NO. We found that exposure to NO increased proliferation of TNBC cells and that treatment with the histone deacetylase inhibitor Vorinostat (SAHA) prevented this proliferation. When histone acetylation was measured in response to NO and/or SAHA, NO significantly decreased acetylation on histone 3 lysine 9 (H3K9ac) and SAHA increased H3K9ac. If NO and SAHA were sequentially administered to cells (in either order), an increase in acetylation was observed in all cases. Mechanistic studies suggest that the "deacetylase" activity of NO does not involve
MeSH term(s)	Acetylation/drug effects ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; Histone Deacetylase Inhibitors/chemistry ; Histone Deacetylase Inhibitors/pharmacology ; Histones/metabolism ; Humans ; Nitric Oxide/metabolism ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Vorinostat/chemistry ; Vorinostat/pharmacology
Chemical Substances	Antineoplastic Agents ; Histone Deacetylase Inhibitors ; Histones ; Nitric Oxide (31C4KY9ESH) ; Vorinostat (58IFB293JI)
Language	English
Publishing date	2021-01-15
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1334659-3
ISSN	1437-4315 ; 1431-6730 ; 1432-0355
ISSN (online)	1437-4315
ISSN	1431-6730 ; 1432-0355
DOI	10.1515/hsz-2020-0323
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Article ; Online: Nitric oxide reduces oxidative stress in cancer cells by forming dinitrosyliron complexes.

Sahni, Sumit / Hickok, Jason R / Thomas, Douglas D

Nitric oxide : biology and chemistry

2018 Volume 76, Page(s) 37–44

Abstract: The chelatable iron pool (CIP) is a small but chemically significant fraction of total cellular iron. While this dynamic population of iron is limited, it is redox active and capable of generating reactive oxygen species (ROS) that can lead to oxidative ... ...

Abstract	The chelatable iron pool (CIP) is a small but chemically significant fraction of total cellular iron. While this dynamic population of iron is limited, it is redox active and capable of generating reactive oxygen species (ROS) that can lead to oxidative stress which is associated with various pathologies. Nitric oxide (•NO), is a free radical signalling molecule that regulates numerous physiological and pathological conditions. We have previously shown that macrophages exposed to endogenously generated or exogenously administered nitric oxide (•NO) results in its interaction with CIP to form dinitrosyliron complexes with thiol containing ligands (DNICs). In this study we assessed the consequences of DNIC formation in cancer cells as •NO is known to be associated with numerous malignancies. Incubation of cancer cells with •NO led to a time and dose dependent increase in formation of DNICs. The formation of DNICs results in the sequestration of the CIP which is a major source of iron for redox reactions and reactive oxygen species (ROS) generation. Therefore, we set out to test the antioxidant effect of •NO by measuring the ability of DNICs to protect cells against oxidative stress. We observed that cancer cells treated with •NO were partially protected against H
MeSH term(s)	Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Survival/drug effects ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Female ; Humans ; Hydrogen Peroxide/antagonists & inhibitors ; Hydrogen Peroxide/metabolism ; Iron/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide/pharmacology ; Nitrogen Oxides/metabolism ; Oxidation-Reduction ; Oxidative Stress/drug effects ; Tumor Cells, Cultured
Chemical Substances	Nitrogen Oxides ; Nitric Oxide (31C4KY9ESH) ; dinitrosyl iron complex (68586-27-6) ; Hydrogen Peroxide (BBX060AN9V) ; Iron (E1UOL152H7)
Language	English
Publishing date	2018-03-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2018.03.003
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Article: Insights into the diverse effects of nitric oxide on tumor biology.

Vasudevan, Divya / Thomas, Douglas D

Vitamins and hormones

2014 Volume 96, Page(s) 265–298

Abstract: Among its many roles in cellular biology, nitric oxide (·NO) has long been associated with cancers both as a protumorigenic and as an antitumorigenic agent. The dual nature of this signaling molecule in varied settings is attributable to its temporal and ...

Abstract	Among its many roles in cellular biology, nitric oxide (·NO) has long been associated with cancers both as a protumorigenic and as an antitumorigenic agent. The dual nature of this signaling molecule in varied settings is attributable to its temporal and concentration-dependent effects that produce different phenotypes. The steady-state ·NO concentration within the cell is a balance between its rate of enzymatic synthesis from the three nitric oxide synthase (NOS) isoforms and consumption via numerous metabolic pathways and demonstrates strong dependence on the tissue oxygen concentration. NOS expression and ·NO production are often deregulated and associated with numerous types of cancers with dissimilar prognostic outcomes. ·NO influences several facets of tumor initiation and progression including DNA damage, chronic inflammation, angiogenesis, epithelial-mesenchymal transition, and metastasis, to name a few. The role of ·NO as an epigenetic modulator has also recently emerged and has potentially important mechanistic implications in regulating transcription of oncogenes and tumor-suppressor genes. ·NO-derived cellular adducts such as dinitrosyliron complexes and the formation of higher nitrogen oxides further alter its cellular behavior. Among anticancer strategies, the use of NOS as a prognostic biomarker and modulation of ·NO production for therapeutic benefit have gained importance over the past decade. Numerous ·NO-releasing drugs and NOS inhibitors have been evaluated in preclinical and clinical settings to arrest tumor growth. Taken together, ·NO affects various arms of cancer signaling networks. An overview of this complex interplay is provided in this chapter.
MeSH term(s)	Gene Expression Regulation, Enzymologic/physiology ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Neoplasms/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide/pharmacology ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase/metabolism ; Oxygen/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Oxygen (S88TT14065)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	201161-x
ISSN	2162-2620 ; 0083-6729
ISSN (online)	2162-2620
ISSN	0083-6729
DOI	10.1016/B978-0-12-800254-4.00011-8
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Article ; Online: Nitric oxide inhibits FTO demethylase activity to regulate N

Kuschman, Hannah Petraitis / Palczewski, Marianne B / Hoffman, Brian / Menhart, Mary / Wang, Xiaowei / Glynn, Sharon / Islam, Abul B M M K / Benevolenskaya, Elizaveta V / Thomas, Douglas D

Redox biology

2023 Volume 67, Page(s) 102928

Abstract: ... ...

Abstract	N
MeSH term(s)	Humans ; Methylation ; Nitric Oxide ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Adenosine/metabolism ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/chemistry ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/metabolism
Chemical Substances	N-methyladenosine (CLE6G00625) ; Nitric Oxide (31C4KY9ESH) ; RNA, Messenger ; Adenosine (K72T3FS567) ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO (EC 1.14.11.33) ; FTO protein, human (EC 1.14.11.33)
Language	English
Publishing date	2023-10-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102928
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Article ; Online: Nitric oxide, the new architect of epigenetic landscapes.

Vasudevan, Divya / Bovee, Rhea C / Thomas, Douglas D

Nitric oxide : biology and chemistry

2016 Volume 59, Page(s) 54–62

Abstract: Nitric oxide (NO) is an endogenously produced signaling molecule with multiple regulatory functions in physiology and disease. The most studied molecular mechanisms underlying the biological functions of NO include its reaction with heme proteins and ... ...

Abstract	Nitric oxide (NO) is an endogenously produced signaling molecule with multiple regulatory functions in physiology and disease. The most studied molecular mechanisms underlying the biological functions of NO include its reaction with heme proteins and regulation of protein activity via modification of thiol residues. A significant number of transcriptional responses and phenotypes observed in NO microenvironments, however, still lack mechanistic understanding. Recent studies shed new light on NO signaling by revealing its influence on epigenetic changes within the cell. Epigenetic alterations are important determinants of transcriptional responses and cell phenotypes, which can relay heritable information during cell division. As transcription across the genome is highly sensitive to these upstream epigenetic changes, this mode of NO signaling provides an alternate explanation for NO-mediated gene expression changes and phenotypes. This review will provide an overview of the interplay between NO and epigenetics as well as emphasize the unprecedented importance of these pathways to explain phenotypic effects associated with biological NO synthesis.
Language	English
Publishing date	2016-09-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2016.08.002
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