文章摘要
Yu Yang,Jun Du,Zhenzhen Hu,Jiaojing Liu,Yinhui Tian,Yichao Zhu,Le Wang,Luo Gu.[J].南京医科大学学报,2011,(4):237~245
Activation of Rac1-PI3K/Akt is required for epidermal growth factor-induced PAK1 activation and cell migration in MDA-MB-231 breast cancer cells
投稿时间:2011-04-12  
DOI:10.7655
中文关键词: 
英文关键词: breast cancer cell, epidermal growth factor, migration, Ras-related C3 botulinum toxin substrate 1 (Rac1), PI3K/Akt, p21-actived kinase (PAK1)
基金项目:
作者单位
Yu Yang Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Jun Du Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Zhenzhen Hu Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Jiaojing Liu Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Yinhui Tian Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Yichao Zhu Cancer Center, Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Le Wang Department of Physiology,Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
Luo Gu Cancer Center, Nanjing Medical University, Nanjing, Jiangsu 210029, China. 
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中文摘要:
      
英文摘要:
      Epidermal growth factor (EGF) may increase cell motility, an event implicated in cancer cell invasion and me-tastasis. However, the underlying mechanisms for EGF-induced cell motility remain elusive. In this study, we found that EGF treatment could activate Ras-related C3 botulinum toxin substrate 1 (Rac1), PI3K/Akt and p21-actived kinase (PAK1) along with cell migration. Ectopic expression of PAK1 K299R, a dominant negative PAK1 mutant, could largely abolish EGF-induced cell migration. Blocking PI3K/Akt signalling with LY294002 or Akt siRNA remarkably inhibited both EGF-induced PAK1 activation and cell migration. Furthermore, expression of dominant-negative Rac1 (T17N) could largely block EGF-induced PI3K/Akt-PAK1 activation and cell migration. Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1. Our study demonstrated that EGF-induced cell migration involves a cascade of signalling events, in-cluding activation of Rac1, generation of ROS and subsequent activation of PI3K/Akt and PAK1.
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