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Unraveling the S-Nitrosylation in Cancer
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Unraveling the S-Nitrosylation in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 17877

Special Issue Editor

Dr. Stephanie Plenchette

E-Mail Website
Guest Editor
1. Laboratoire d'Immunologie et Immunothérapie des Cancers (LIIC), EPHE, PSL Research University, 75000 Paris, France
2. LIIC, EA7269, université de Bourgogne Franche-Comté, 21000 Dijon, France
Interests: nitric oxide; cancer; S-nitrosylation; signaling pathways; tumor microenvironment; inflammation; immune cells; chemotherapy

Special Issue Information

Dear Colleagues,

Nitric oxide (NO) plays a substantial role in various physiological and pathophysiological systems, including cancer. The dichotomous consequences of NO on cancer, both pro-tumoral and anti-tumoral, represent a dilemma that still raises questions. S-Nitrosylation, the oxidation of cysteine thiol residues by NO to form S-nitrosothiols, is a fundamental redox-based regulatory mechanism that highly influences not only NO-mediated biological activities in cancer but also most aspects of cell biology. As a major NO-based post-translation modification, S-nitrosylation can modify a wide variety of target protein functions, largely influencing cellular signaling outcomes. S-Nitrosylation is a reversible protein post-translation modification and a dynamic process that can exert opposite effects on cancer disease. A deep understanding of protein S-nitrosylation in signaling pathways, and in a cell-context-dependent manner, is critically needed in order to further unravel the pleotropic effects of S-nitrosylation in tumor biology for future therapeutic perspectives.

This Special Issue of the International Journal of Molecular Sciences aims to contribute with original scientific research articles and review articles to report recent findings and knowledge on S-nitrosylation with emphasis on the fundamental aspects of malignant cells across all types of cancer. Topics of interest include, but are not limited to, tumor promotion, tumor growth, epithelial–mesenchymal transition, angiogenesis, metastasis, and regulation of cell death pathways. We also welcome contributions focusing on the investigation of proteins that are prone to regulation by S-nitrosylation (balance between S-nitrosylation and denitrosylation, transnitrosylation, and experimental techniques for analyzing S-nitrosylation and/or S-nitrosoproteome) in the field of cancer research. 

Dr. Stephanie Plenchette
Guest Editor

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Keywords

  • Nitric oxide
  • Cancer
  • S-Nitrosylation
  • Transnitrosylation
  • Cellular signaling
  • Tumor development
  • Cell survival
  • Cell death
  • S-Nitrosoproteome

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Published Papers (3 papers)

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17 pages, 13028 KiB  
Article
Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells
by Sarra Bouaouiche, Silvia Ghione, Randa Sghaier, Olivier Burgy, Cindy Racoeur, Valentin Derangère, Ali Bettaieb and Stéphanie Plenchette
Int. J. Mol. Sci. 2021, 22(16), 8449; https://doi.org/10.3390/ijms22168449 - 6 Aug 2021
Cited by 10 | Viewed by 2423
Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a [...] Read more.
Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a main upstream activator of the JAK2/STAT3 pathway. In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments. We used a subtoxic dose of carboplatin and/or recombinant IL-6 to activate the JAK2/STAT3 signaling pathway and its functional outcomes. We found an inhibitory effect of GTN on the activation of the JAK2/STAT3 signaling, migration and invasion of TNBC cells. We discovered that GTN inhibits the activation of JAK2, the upstream activator of STAT3, and mediates the S-nitrosylation of JAK2. Finally, the effect of GTN (Nitronal) on lung metastasis was investigated to assess its antitumor activity in vivo. Full article
(This article belongs to the Special Issue Unraveling the S-Nitrosylation in Cancer)
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Review

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32 pages, 2527 KiB  
Review
S-Nitrosylation in Tumor Microenvironment
by Vandana Sharma, Veani Fernando, Joshua Letson, Yashna Walia, Xunzhen Zheng, Daniel Fackelman and Saori Furuta
Int. J. Mol. Sci. 2021, 22(9), 4600; https://doi.org/10.3390/ijms22094600 - 27 Apr 2021
Cited by 26 | Viewed by 6886
Abstract
S-nitrosylation is a selective and reversible post-translational modification of protein thiols by nitric oxide (NO), which is a bioactive signaling molecule, to exert a variety of effects. These effects include the modulation of protein conformation, activity, stability, and protein-protein interactions. S-nitrosylation plays a [...] Read more.
S-nitrosylation is a selective and reversible post-translational modification of protein thiols by nitric oxide (NO), which is a bioactive signaling molecule, to exert a variety of effects. These effects include the modulation of protein conformation, activity, stability, and protein-protein interactions. S-nitrosylation plays a central role in propagating NO signals within a cell, tissue, and tissue microenvironment, as the nitrosyl moiety can rapidly be transferred from one protein to another upon contact. This modification has also been reported to confer either tumor-suppressing or tumor-promoting effects and is portrayed as a process involved in every stage of cancer progression. In particular, S-nitrosylation has recently been found as an essential regulator of the tumor microenvironment (TME), the environment around a tumor governing the disease pathogenesis. This review aims to outline the effects of S-nitrosylation on different resident cells in the TME and the diverse outcomes in a context-dependent manner. Furthermore, we will discuss the therapeutic potentials of modulating S-nitrosylation levels in tumors. Full article
(This article belongs to the Special Issue Unraveling the S-Nitrosylation in Cancer)
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30 pages, 2759 KiB  
Review
The Role of Nitric Oxide in Cancer: Master Regulator or NOt?
by Faizan H. Khan, Eoin Dervan, Dibyangana D. Bhattacharyya, Jake D. McAuliffe, Katrina M. Miranda and Sharon A. Glynn
Int. J. Mol. Sci. 2020, 21(24), 9393; https://doi.org/10.3390/ijms21249393 - 10 Dec 2020
Cited by 105 | Viewed by 7974
Abstract
Nitric oxide (NO) is a key player in both the development and suppression of tumourigenesis depending on the source and concentration of NO. In this review, we discuss the mechanisms by which NO induces DNA damage, influences the DNA damage repair response, and [...] Read more.
Nitric oxide (NO) is a key player in both the development and suppression of tumourigenesis depending on the source and concentration of NO. In this review, we discuss the mechanisms by which NO induces DNA damage, influences the DNA damage repair response, and subsequently modulates cell cycle arrest. In some circumstances, NO induces cell cycle arrest and apoptosis protecting against tumourigenesis. NO in other scenarios can cause a delay in cell cycle progression, allowing for aberrant DNA repair that promotes the accumulation of mutations and tumour heterogeneity. Within the tumour microenvironment, low to moderate levels of NO derived from tumour and endothelial cells can activate angiogenesis and epithelial-to-mesenchymal transition, promoting an aggressive phenotype. In contrast, high levels of NO derived from inducible nitric oxide synthase (iNOS) expressing M1 and Th1 polarised macrophages and lymphocytes may exert an anti-tumour effect protecting against cancer. It is important to note that the existing evidence on immunomodulation is mainly based on murine iNOS studies which produce higher fluxes of NO than human iNOS. Finally, we discuss different strategies to target NO related pathways therapeutically. Collectively, we present a picture of NO as a master regulator of cancer development and progression. Full article
(This article belongs to the Special Issue Unraveling the S-Nitrosylation in Cancer)
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