NOD-like receptor signaling in inflammation-associated cancers : From functions to targeted therapies
Copyright © 2019 Elsevier GmbH. All rights reserved..
BACKGROUND: Recently, many studies have reported that some botanicals and natural products were able to regulate NOD-like receptor signaling. NOD-like receptors (NLRs) have been established as crucial regulators in inflammation-associated tumorigenesis, angiogenesis, cancer cell stemness and chemoresistance. NLRs specifically sense pathogen-associated molecular patterns and respond by activating other signaling regulators, including Rip2 kinase, NF-κB, MAPK and ASC/caspase-1, leading to the secretion of various cytokines.
PURPOSE: The aim of this article is to review the molecular mechanisms of NOD-like receptor signaling in inflammation-associated cancers and the NLRs-targeted botanicals and synthetic small molecules in cancer intervention.
RESULTS: Aberrant activation of NLRs occurs in various cancers, orchestrating the tissue microenvironment and potentiating neoplastic risk. Blocking NLR inflammasome activation by botanicals or synthetic small molecules may be a valuable way to prevent cancer progression. Moreover, due to the roles of NLRs in regulating cytokine production, NLR signaling may be correlated with senescence-associated secretory phenotype.
CONCLUSION: In this review, we discuss how NLR signaling is involved in inflammation-associated cancers, and highlight the NLR-targeted botanicals and synthetic small molecules in cancer intervention.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:64 |
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Enthalten in: |
Phytomedicine : international journal of phytotherapy and phytopharmacology - 64(2019) vom: 15. Nov., Seite 152925 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Liu, Peng [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 02.03.2020 Date Revised 02.03.2020 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.phymed.2019.152925 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM300753748 |
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520 | |a BACKGROUND: Recently, many studies have reported that some botanicals and natural products were able to regulate NOD-like receptor signaling. NOD-like receptors (NLRs) have been established as crucial regulators in inflammation-associated tumorigenesis, angiogenesis, cancer cell stemness and chemoresistance. NLRs specifically sense pathogen-associated molecular patterns and respond by activating other signaling regulators, including Rip2 kinase, NF-κB, MAPK and ASC/caspase-1, leading to the secretion of various cytokines | ||
520 | |a PURPOSE: The aim of this article is to review the molecular mechanisms of NOD-like receptor signaling in inflammation-associated cancers and the NLRs-targeted botanicals and synthetic small molecules in cancer intervention | ||
520 | |a RESULTS: Aberrant activation of NLRs occurs in various cancers, orchestrating the tissue microenvironment and potentiating neoplastic risk. Blocking NLR inflammasome activation by botanicals or synthetic small molecules may be a valuable way to prevent cancer progression. Moreover, due to the roles of NLRs in regulating cytokine production, NLR signaling may be correlated with senescence-associated secretory phenotype | ||
520 | |a CONCLUSION: In this review, we discuss how NLR signaling is involved in inflammation-associated cancers, and highlight the NLR-targeted botanicals and synthetic small molecules in cancer intervention | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Li, Ruyan |e verfasserin |4 aut | |
700 | 1 | |a Liang, Zhiquan |e verfasserin |4 aut | |
700 | 1 | |a Shen, Mingxiang |e verfasserin |4 aut | |
700 | 1 | |a Xu, Han |e verfasserin |4 aut | |
700 | 1 | |a Ren, Dewan |e verfasserin |4 aut | |
700 | 1 | |a Ji, Mengchen |e verfasserin |4 aut | |
700 | 1 | |a Yuan, Sirui |e verfasserin |4 aut | |
700 | 1 | |a Shang, Dongsheng |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Yibang |e verfasserin |4 aut | |
700 | 1 | |a Liu, Hanqing |e verfasserin |4 aut | |
700 | 1 | |a Tu, Zhigang |e verfasserin |4 aut | |
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