SDF-1/CXCR4 Axis Regulates Cell Cycle Progression and Epithelial-Mesenchymal Transition via Up-regulation of Survivin in Glioblastoma

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• 作者：Anyan Liao ; Ranran Shi ; Yuliang Jiang ; Suqing Tian ; Panpan Li…
• 关键词：SDF ; 1/CXCR4 ; Survivin ; Cell cycle progression ; EMT
• 刊名：Molecular Neurobiology
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：53
• 期：1
• 页码：210-215
• 全文大小：387 KB
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• 作者单位：Anyan Liao (1)
  Ranran Shi (2)
  Yuliang Jiang (1)
  Suqing Tian (1)
  Panpan Li (3)
  Fuxi Song (3)
  Yalan Qu (3)
  Jinna Li (1)
  Haiqin Yun (4)
  Xiangshan Yang (5)
  
  1. Department of Radiation Oncology, Peking University 3rd Hospital, No. 49 Hua Yuan Bei Lu, Beijing, 100191, China
  2. Department of General Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China
  3. Shandong University School of Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, China
  4. Department of Pathology, Qilu Hospital of Shandong University, Jinan, Shandong, China
  5. Department of Pathology, Affiliated Hospital of Shandong Academy of Medical Sciences, Jinan, Shandong, China
  
• 刊物主题：Neurosciences; Neurobiology; Cell Biology; Neurology;
• 出版者：Springer US
• ISSN：1559-1182

文摘

Stromal cell-derived factor 1 (SDF-1)/CXCR4 ligand-receptor axis is widely recommended as an attractive target for cancer therapy. Meanwhile, epithelial-mesenchymal transition (EMT) process is linked to disease pathophysiology. As one of inhibitors of apoptosis proteins, survivin is implicated in the onset and development of cancer. In the present study, we tried to determine the cause-effect associations between SDF-1/CXCR4 axis and survivin expression in glioblastoma U-251 cell line. Survivin activation and inhibition were induced with exogenous SDF-1 and survivin small interfering RNA (survivin siRNA), respectively. Western blot was used to detect relevant proteins in SDF-1/CXCR4 axis. Western blot analysis revealed that survivin expression in U-251 increased in a dose- and time-dependent manner in response to SDF-1 treatment. However, the interference with MEK/ERK and PI3K/AKT pathway prohibited SDF-1-induced survivin up-regulation. Importantly, survivin knockdown abrogated cell cycle progression and the expression of snail and N-cadherin, compared with non-transfectants. In conclusion, the present study shows that SDF-1 up-regulates survivin via MEK/ERK and PI3K/AKT pathway, leading to cell cycle progression and EMT occurrence dependent on survivin. The blockade of survivin will allow for the treatment of glioblastoma.