4.6

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2.2

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  • ISSN 1674-8301
  • CN 32-1810/R
Yu Yang, Jun Du, Zhenzhen Hu, Jiaojing Liu, Yinhui Tian, Yichao Zhu, Le Wang, Luo Gu. Activation of Rac1-PI3K/Akt is required for epidermal growth factor-induced PAK1 activation and cell migration in MDA-MB-231 breast cancer cells[J]. The Journal of Biomedical Research, 2011, 25(4): 237-245. DOI: 10.1016/S1674-8301(11)60032-8
Citation: Yu Yang, Jun Du, Zhenzhen Hu, Jiaojing Liu, Yinhui Tian, Yichao Zhu, Le Wang, Luo Gu. Activation of Rac1-PI3K/Akt is required for epidermal growth factor-induced PAK1 activation and cell migration in MDA-MB-231 breast cancer cells[J]. The Journal of Biomedical Research, 2011, 25(4): 237-245. DOI: 10.1016/S1674-8301(11)60032-8

Activation of Rac1-PI3K/Akt is required for epidermal growth factor-induced PAK1 activation and cell migration in MDA-MB-231 breast cancer cells

Funds: 

This work was supported by grants from the National Natural Science Foundation of China (No. 30872926) and the Program for Advanced Talents within Six Industries of Jiangsu Province (08-D) to Dr. Luo Gu

the Science Development Foundation of Nanjing Medical Univer-sity (No. 2010NJMUZ35) and the Research Program funded by School of Basic Medical Science, Nanjing Medical University to Dr. Jun Du.

More Information
  • Received Date: April 11, 2011
  • 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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