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NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals
Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Cognizant Communication Corporation
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848456/ https://www.ncbi.nlm.nih.gov/pubmed/29769161 http://dx.doi.org/10.3727/096504018X15264647024196 |
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author | Xue, Liping Lu, Bin Gao, Bibo Shi, Yangyang Xu, Jingqi Yang, Rui Xu, Bo Ding, Peng |
author_facet | Xue, Liping Lu, Bin Gao, Bibo Shi, Yangyang Xu, Jingqi Yang, Rui Xu, Bo Ding, Peng |
author_sort | Xue, Liping |
collection | PubMed |
description | Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1β, IL-1β antibody, and NF-κB inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected by PCR, Western blot, and ELISA. NLRP3 and NF-κB p65 increased and were positively correlated in glioma tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1β and NF-κB p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous IL-1β-elevated cell proliferation and invasion, whereas IL-1β elimination impaired the proproliferation effect of NLRP3 hyperexpression. Furthermore, NF-κB blockage abrogated IL-1β and NLRP3 hyperexpression increased cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1β/NF-κB p65 signals. |
format | Online Article Text |
id | pubmed-7848456 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Cognizant Communication Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-78484562021-02-16 NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals Xue, Liping Lu, Bin Gao, Bibo Shi, Yangyang Xu, Jingqi Yang, Rui Xu, Bo Ding, Peng Oncol Res Article Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1β, IL-1β antibody, and NF-κB inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected by PCR, Western blot, and ELISA. NLRP3 and NF-κB p65 increased and were positively correlated in glioma tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1β and NF-κB p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous IL-1β-elevated cell proliferation and invasion, whereas IL-1β elimination impaired the proproliferation effect of NLRP3 hyperexpression. Furthermore, NF-κB blockage abrogated IL-1β and NLRP3 hyperexpression increased cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1β/NF-κB p65 signals. Cognizant Communication Corporation 2019-05-07 /pmc/articles/PMC7848456/ /pubmed/29769161 http://dx.doi.org/10.3727/096504018X15264647024196 Text en Copyright © 2019 Cognizant, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License. |
spellingShingle | Article Xue, Liping Lu, Bin Gao, Bibo Shi, Yangyang Xu, Jingqi Yang, Rui Xu, Bo Ding, Peng NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title | NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title_full | NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title_fullStr | NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title_full_unstemmed | NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title_short | NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals |
title_sort | nlrp3 promotes glioma cell proliferation and invasion via the interleukin-1β/nf-κb p65 signals |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848456/ https://www.ncbi.nlm.nih.gov/pubmed/29769161 http://dx.doi.org/10.3727/096504018X15264647024196 |
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