A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells

Nitric oxide (NO) works as a signaling molecule, toxicant, and antioxidant in the body’s physiological and pathological processes. JS-K is designed to be activated by glutathione-S-transferase (GST) and release NO in a sustained and controlled manner within the tumor cells. JS-K also promotes apopto...

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Detalles Bibliográficos
Autores principales: Tan, Guobin, Wu, Aiming, Li, Zhiqin, Awasthi, Prashant
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2019
Materias:
Review Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797525/
https://www.ncbi.nlm.nih.gov/pubmed/35116903
http://dx.doi.org/10.21037/tcr.2019.07.20
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author Tan, Guobin
Wu, Aiming
Li, Zhiqin
Awasthi, Prashant
author_facet Tan, Guobin
Wu, Aiming
Li, Zhiqin
Awasthi, Prashant
author_sort Tan, Guobin
collection PubMed
description Nitric oxide (NO) works as a signaling molecule, toxicant, and antioxidant in the body’s physiological and pathological processes. JS-K is designed to be activated by glutathione-S-transferase (GST) and release NO in a sustained and controlled manner within the tumor cells. JS-K also promotes apoptosis in cancer cells through mitogen-activated protein kinase (MAPK) pathway, ubiquitin-proteasome pathway, cell factor β-catenin/T (TCF) signaling pathway, and other mechanisms. In future studies, we should further develop new NO precursors, so that new drugs in the treatment of cancer can become more efficient, more accurate, and have less adverse reactions.
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spelling pubmed-87975252022-02-02 A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells Tan, Guobin Wu, Aiming Li, Zhiqin Awasthi, Prashant Transl Cancer Res Review Article Nitric oxide (NO) works as a signaling molecule, toxicant, and antioxidant in the body’s physiological and pathological processes. JS-K is designed to be activated by glutathione-S-transferase (GST) and release NO in a sustained and controlled manner within the tumor cells. JS-K also promotes apoptosis in cancer cells through mitogen-activated protein kinase (MAPK) pathway, ubiquitin-proteasome pathway, cell factor β-catenin/T (TCF) signaling pathway, and other mechanisms. In future studies, we should further develop new NO precursors, so that new drugs in the treatment of cancer can become more efficient, more accurate, and have less adverse reactions. AME Publishing Company 2019-08 /pmc/articles/PMC8797525/ /pubmed/35116903 http://dx.doi.org/10.21037/tcr.2019.07.20 Text en 2019 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
spellingShingle Review Article
Tan, Guobin
Wu, Aiming
Li, Zhiqin
Awasthi, Prashant
A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title_full A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title_fullStr A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title_full_unstemmed A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title_short A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells
title_sort review of the relatively complex mechanism of js-k induced apoptosis in cancer cells
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797525/
https://www.ncbi.nlm.nih.gov/pubmed/35116903
http://dx.doi.org/10.21037/tcr.2019.07.20
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