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Am J Physiol Cell Physiol (September 10, 2003). doi:10.1152/ajpcell.00142.2003
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Submitted on April 9, 2003
Accepted on September 5, 2003

PI3K induced actin filament remodeling through Akt and p70S6K1: implication of essential role in cell migration

Yong Qian1, Linda Corum2, Qiao Meng2, John Blenis3, Jenny Z Zheng2, Xianglin Shi4, Daniel C Flynn2, and Bing-Hua Jiang2*

1 Pathology and Physiology, NIOSH, Morgantown, WV, USA; MBR Cancer Center, West Virginia University, Morgantown, WV, USA
2 MBR Cancer Center, West Virginia University, Morgantown, WV, USA
3 Cell Biology, Harvard Medical School, Boston, MA, USA
4 Pathology and Physiology, NIOSH, Morgantown, WV, USA

* To whom correspondence should be addressed. E-mail: bhjiang{at}hsc.wvu.edu.

This study was designed to identify the molecular mechanisms of PI3K-inducecd actin filament remodeling and cell migration. Expression of active forms of PI3K, v-P3k or Myr-P3k, was sufficient to induce actin filament remodeling to lead to an increase in cell migration, as well as the activation of Akt in chicken embryo fibroblast (CEF) cells. Either the inhibition of PI3K activity using a PI3K specific inhibitor LY294002, or the disruption of Akt activity restored the integrity of actin filaments in CEF cells and inhibited PI3K-inudced cell migration. We also found that expression of an activated form of Akt (Myr-Akt) was sufficient to remodel actin filaments to lead to an increase in cell migration, which was unable to be inhibited by the presence of LY294002. Furthermore, we found p70S6K1 kinase was a downstream molecule that can mediate the effects of both PI3K and Akt on actin filaments and cell migration. Overexpression of an active form of p70S6K1 was sufficient to induce actin filament remodeling and cell migration in CEF cells. These results demonstrate that activation of PI3K activity alone is sufficient to remodel actin filaments to increase cell migration through the activation of Akt and p70S6K1 in CEF cells.




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