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S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up‐regulated in GBM t...

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Autores principales: Tu, Yiming, Xie, Peng, Du, Xiaoliu, Fan, Liang, Bao, Zhongyuan, Sun, Guangchi, zhao, Pengzhan, Chao, Honglu, Li, Chong, Zeng, Ailiang, Pan, Minhong, Ji, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787445/
https://www.ncbi.nlm.nih.gov/pubmed/31430050
http://dx.doi.org/10.1111/jcmm.14574
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author Tu, Yiming
Xie, Peng
Du, Xiaoliu
Fan, Liang
Bao, Zhongyuan
Sun, Guangchi
zhao, Pengzhan
Chao, Honglu
Li, Chong
Zeng, Ailiang
Pan, Minhong
Ji, Jing
author_facet Tu, Yiming
Xie, Peng
Du, Xiaoliu
Fan, Liang
Bao, Zhongyuan
Sun, Guangchi
zhao, Pengzhan
Chao, Honglu
Li, Chong
Zeng, Ailiang
Pan, Minhong
Ji, Jing
author_sort Tu, Yiming
collection PubMed
description Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up‐regulated in GBM tissues and higher S100A11 expression indicated poor prognosis of GBM patients. Overexpression of S100A11 promoted GBM cell growth, epithelial‐mesenchymal transition (EMT), migration, invasion and generation of glioma stem cells (GSCs), whereas its knockdown inhibited these activities. More importantly, S100A11 interacted with ANXA2 and regulated NF‐κB signalling pathway through decreasing ubiquitination and degradation of ANXA2. Additionally, NF‐κB regulated S100A11 at transcriptional level as a positive feedback. We also demonstrated the S100A11 on tumour growth in GBM using an orthotopic tumour xenografting. These data demonstrate that S100A11/ANXA2/NF‐κB positive feedback loop in GBM cells that promote the progression of GBM.
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spelling pubmed-67874452019-10-17 S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop Tu, Yiming Xie, Peng Du, Xiaoliu Fan, Liang Bao, Zhongyuan Sun, Guangchi zhao, Pengzhan Chao, Honglu Li, Chong Zeng, Ailiang Pan, Minhong Ji, Jing J Cell Mol Med Original Articles Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up‐regulated in GBM tissues and higher S100A11 expression indicated poor prognosis of GBM patients. Overexpression of S100A11 promoted GBM cell growth, epithelial‐mesenchymal transition (EMT), migration, invasion and generation of glioma stem cells (GSCs), whereas its knockdown inhibited these activities. More importantly, S100A11 interacted with ANXA2 and regulated NF‐κB signalling pathway through decreasing ubiquitination and degradation of ANXA2. Additionally, NF‐κB regulated S100A11 at transcriptional level as a positive feedback. We also demonstrated the S100A11 on tumour growth in GBM using an orthotopic tumour xenografting. These data demonstrate that S100A11/ANXA2/NF‐κB positive feedback loop in GBM cells that promote the progression of GBM. John Wiley and Sons Inc. 2019-08-20 2019-10 /pmc/articles/PMC6787445/ /pubmed/31430050 http://dx.doi.org/10.1111/jcmm.14574 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Tu, Yiming
Xie, Peng
Du, Xiaoliu
Fan, Liang
Bao, Zhongyuan
Sun, Guangchi
zhao, Pengzhan
Chao, Honglu
Li, Chong
Zeng, Ailiang
Pan, Minhong
Ji, Jing
S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title_full S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title_fullStr S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title_full_unstemmed S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title_short S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop
title_sort s100a11 functions as novel oncogene in glioblastoma via s100a11/anxa2/nf‐κb positive feedback loop
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787445/
https://www.ncbi.nlm.nih.gov/pubmed/31430050
http://dx.doi.org/10.1111/jcmm.14574
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