作者: Yu Yang , Jun Du , Zhenzhen Hu , Jiaojing Liu , Yinhui Tian
DOI: 10.1016/S1674-8301(11)60032-8
关键词: Cancer research 、 PI3K/AKT/mTOR pathway 、 Epidermal growth factor 、 Cancer cell 、 Cell migration 、 RAC1 、 Protein kinase B 、 Motility 、 Kinase 、 Biology
摘要: Epidermal growth factor (EGF) may increase cell motility, an event implicated in cancer invasion and metastasis. However, the underlying mechanisms for EGF-induced motility remain elusive. In this study, we found that EGF treatment could activate Ras-related C3 botulinum toxin substrate 1 (Rac1), PI3K/Akt p21-actived kinase (PAK1) along with migration. Ectopic expression of PAK1 K299R, a dominant negative mutant, largely abolish Blocking signalling LY294002 or Akt siRNA remarkably inhibited both activation Furthermore, dominant-negative Rac1 (T17N) block PI3K/Akt-PAK1 Interestingly, induce significant production ROS, N-acetyl-L-cysteine, scavenger ROS which abolished generation, migration, as well PAK, but not Rac1. Our study demonstrated migration involves cascade events, including Rac1, generation subsequent PAK1.