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The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation

IL-33 is an important member of the IL-1 family which has pleiotropic activities in innate and adaptive immune responses. Recently, some researchers have focused on the function of cellular immunity in the development of tumor. The biological role of IL-33 in glioma is poorly understood. In this stu...

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Detalles Bibliográficos
Autores principales: Lin, Lin, Li, Yang, Liu, Mingli, Li, Qingbin, Liu, Quan, Li, Ruiyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053587/
https://www.ncbi.nlm.nih.gov/pubmed/32003751
http://dx.doi.org/10.18632/aging.102707
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author Lin, Lin
Li, Yang
Liu, Mingli
Li, Qingbin
Liu, Quan
Li, Ruiyan
author_facet Lin, Lin
Li, Yang
Liu, Mingli
Li, Qingbin
Liu, Quan
Li, Ruiyan
author_sort Lin, Lin
collection PubMed
description IL-33 is an important member of the IL-1 family which has pleiotropic activities in innate and adaptive immune responses. Recently, some researchers have focused on the function of cellular immunity in the development of tumor. The biological role of IL-33 in glioma is poorly understood. In this study, we showed that glioma cells and tissues expressed higher levels of IL-33 and its receptor ST2 compared to normal brain. Clinically, IL-33 expression was associated with poor survival in patients with glioma. Administration of human IL-33 enhanced cell migration, invasion, epithelial to mesenchymal transition and stemness. Anti-ST2 blocked these effects of IL-33 on tumor. Mechanistically, IL-33 activated JNK signaling pathway via ST2 and increased the expression of key transcription factors that controlled the process of EMT and stemness. Moreover, IL-33 prevented temozolomide induced tumor apoptosis. Anti-ST2 or knockdown IL-33 increased the sensitivity of tumor to temozolomide. Thus, targeting the IL-33/ST2 axis may offer an opportunity to the treatment of glioma patients.
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spelling pubmed-70535872020-03-12 The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation Lin, Lin Li, Yang Liu, Mingli Li, Qingbin Liu, Quan Li, Ruiyan Aging (Albany NY) Research Paper IL-33 is an important member of the IL-1 family which has pleiotropic activities in innate and adaptive immune responses. Recently, some researchers have focused on the function of cellular immunity in the development of tumor. The biological role of IL-33 in glioma is poorly understood. In this study, we showed that glioma cells and tissues expressed higher levels of IL-33 and its receptor ST2 compared to normal brain. Clinically, IL-33 expression was associated with poor survival in patients with glioma. Administration of human IL-33 enhanced cell migration, invasion, epithelial to mesenchymal transition and stemness. Anti-ST2 blocked these effects of IL-33 on tumor. Mechanistically, IL-33 activated JNK signaling pathway via ST2 and increased the expression of key transcription factors that controlled the process of EMT and stemness. Moreover, IL-33 prevented temozolomide induced tumor apoptosis. Anti-ST2 or knockdown IL-33 increased the sensitivity of tumor to temozolomide. Thus, targeting the IL-33/ST2 axis may offer an opportunity to the treatment of glioma patients. Impact Journals 2020-01-29 /pmc/articles/PMC7053587/ /pubmed/32003751 http://dx.doi.org/10.18632/aging.102707 Text en Copyright © 2020 Lin et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Lin, Lin
Li, Yang
Liu, Mingli
Li, Qingbin
Liu, Quan
Li, Ruiyan
The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title_full The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title_fullStr The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title_full_unstemmed The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title_short The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
title_sort interleukin-33/st2 axis promotes glioma mesenchymal transition, stemness and tmz resistance via jnk activation
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053587/
https://www.ncbi.nlm.nih.gov/pubmed/32003751
http://dx.doi.org/10.18632/aging.102707
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