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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.
Afiliación
  • Tu Y; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Xie P; Department of Neurosurgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, The Second People's Hospital of Huai'an, Huai'an, China.
  • Du X; Department of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Fan L; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Bao Z; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Sun G; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Zhao P; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Chao H; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Li C; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Zeng A; Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • Pan M; Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
  • Ji J; Department of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
J Cell Mol Med ; 23(10): 6907-6918, 2019 10.
Article en En | MEDLINE | ID: mdl-31430050
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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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Oncogenes / Neoplasias Encefálicas / Proteínas S100 / FN-kappa B / Anexina A2 / Glioblastoma / Retroalimentación Fisiológica Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2019 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Oncogenes / Neoplasias Encefálicas / Proteínas S100 / FN-kappa B / Anexina A2 / Glioblastoma / Retroalimentación Fisiológica Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2019 Tipo del documento: Article País de afiliación: China