S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop. Issue 10 (20th August 2019)

• Record Type: Journal Article
• Authors: Tu, Yiming; Xie, Peng; Du, Xiaoliu; Fan, Liang; Bao, Zhongyuan; Sun, Guangchi; zhao, Pengzhan; Chao, Honglu; Li, Chong; Zeng, Ailiang; Pan, Minhong; Ji, Jing
• Is Part Of: Journal of cellular and molecular medicine. Volume 23:Issue 10(2019)
• Page Start: 6907
• Page End: 6918
• Publication Date: 2019-08-20
• Subjects: ANXA2 -- glioblastoma -- NF‐κB -- S100A11 -- ubiquitination; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.14574
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: 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.