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Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer
Inflammation plays a major role in the development and progression of breast cancer(BC). Proliferation, invasion, angiogenesis, and metastasis are all linked to inflammation and tumorigenesis. Furthermore, tumor microenvironment (TME) inflammation-mediated cytokine releases play a critical role in t...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Springer US
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10257378/ https://www.ncbi.nlm.nih.gov/pubmed/37300757 http://dx.doi.org/10.1007/s12672-023-00701-7 |
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author | Wang, Xixi Lin, Junyi Wang, Zhe Li, Zhi Wang, Minghua |
author_facet | Wang, Xixi Lin, Junyi Wang, Zhe Li, Zhi Wang, Minghua |
author_sort | Wang, Xixi |
collection | PubMed |
description | Inflammation plays a major role in the development and progression of breast cancer(BC). Proliferation, invasion, angiogenesis, and metastasis are all linked to inflammation and tumorigenesis. Furthermore, tumor microenvironment (TME) inflammation-mediated cytokine releases play a critical role in these processes. By recruiting caspase-1 through an adaptor apoptosis-related spot protein, inflammatory caspases are activated by the triggering of pattern recognition receptors on the surface of immune cells. Toll-like receptors, NOD-like receptors, and melanoma-like receptors are not triggered. It activates the proinflammatory cytokines interleukin (IL)-1β and IL-18 and is involved in different biological processes that exert their effects. The Nod-Like Receptor Protein 3 (NLRP3) inflammasome regulates inflammation by mediating the secretion of proinflammatory cytokines and interacting with other cellular compartments through the inflammasome's central role in innate immunity. NLRP3 inflammasome activation mechanisms have received much attention in recent years. Inflammatory diseases including enteritis, tumors, gout, neurodegenerative diseases, diabetes, and obesity are associated with abnormal activation of the NLRP3 inflammasome. Different cancer diseases have been linked to NLRP3 and its role in tumorigenesis may be the opposite. Tumors can be suppressed by it, as has been seen primarily in the context of colorectal cancer associated with colitis. However, cancers such as gastric and skin can also be promoted by it. The inflammasome NLRP3 is associated with breast cancer, but there are few specific reviews. This review focuses on the structure, biological characteristics and mechanism of inflammasome, the relationship between NLRP3 in breast cancer Non-Coding RNAs, MicroRNAs and breast cancer microenvironment, especially the role of NLRP3 in triple-negative breast cancer (TNBC). And the potential strategies of using NLRP3 inflammasome to target breast cancer, such as NLRP3-based nanoparticle technology and gene target therapy, are reviewed. |
format | Online Article Text |
id | pubmed-10257378 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-102573782023-06-12 Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer Wang, Xixi Lin, Junyi Wang, Zhe Li, Zhi Wang, Minghua Discov Oncol Review Inflammation plays a major role in the development and progression of breast cancer(BC). Proliferation, invasion, angiogenesis, and metastasis are all linked to inflammation and tumorigenesis. Furthermore, tumor microenvironment (TME) inflammation-mediated cytokine releases play a critical role in these processes. By recruiting caspase-1 through an adaptor apoptosis-related spot protein, inflammatory caspases are activated by the triggering of pattern recognition receptors on the surface of immune cells. Toll-like receptors, NOD-like receptors, and melanoma-like receptors are not triggered. It activates the proinflammatory cytokines interleukin (IL)-1β and IL-18 and is involved in different biological processes that exert their effects. The Nod-Like Receptor Protein 3 (NLRP3) inflammasome regulates inflammation by mediating the secretion of proinflammatory cytokines and interacting with other cellular compartments through the inflammasome's central role in innate immunity. NLRP3 inflammasome activation mechanisms have received much attention in recent years. Inflammatory diseases including enteritis, tumors, gout, neurodegenerative diseases, diabetes, and obesity are associated with abnormal activation of the NLRP3 inflammasome. Different cancer diseases have been linked to NLRP3 and its role in tumorigenesis may be the opposite. Tumors can be suppressed by it, as has been seen primarily in the context of colorectal cancer associated with colitis. However, cancers such as gastric and skin can also be promoted by it. The inflammasome NLRP3 is associated with breast cancer, but there are few specific reviews. This review focuses on the structure, biological characteristics and mechanism of inflammasome, the relationship between NLRP3 in breast cancer Non-Coding RNAs, MicroRNAs and breast cancer microenvironment, especially the role of NLRP3 in triple-negative breast cancer (TNBC). And the potential strategies of using NLRP3 inflammasome to target breast cancer, such as NLRP3-based nanoparticle technology and gene target therapy, are reviewed. Springer US 2023-06-10 /pmc/articles/PMC10257378/ /pubmed/37300757 http://dx.doi.org/10.1007/s12672-023-00701-7 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Wang, Xixi Lin, Junyi Wang, Zhe Li, Zhi Wang, Minghua Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title | Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title_full | Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title_fullStr | Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title_full_unstemmed | Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title_short | Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer |
title_sort | possible therapeutic targets for nlrp3 inflammasome-induced breast cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10257378/ https://www.ncbi.nlm.nih.gov/pubmed/37300757 http://dx.doi.org/10.1007/s12672-023-00701-7 |
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