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MBC in Press, published online ahead of print January 23, 2008
Mol. Biol. Cell 10.1091/mbc.E07-08-0753

A more recent version of this article appeared on April 1, 2008
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Submitted on August 3, 2007
Revised on November 28, 2007
Accepted on January 10, 2008

Disruption of c-Jun Reduces Cellular Migration and Invasion through Inhibition of c-Src and Hyperactivation of ROCK II Kinase

Xuanmao Jiao,* Sanjay Katiyar,*{dagger} Manran Liu,*{dagger} Susette C. Mueller,{ddagger} Michael P. Lisanti,* Anping Li,* Timothy G. Pestell,* Kongming Wu,* Xiaoming Ju,* Zhiping Li,* Erwin F. Wagner,{sect} Tatsuo Takeya,|| Chenguang Wang,*¶ and Richard G. Pestell*¶

Departments of *Cancer Biology and Medical Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107; {ddagger}Georgetown University, Lombardi Comprehensive Cancer Center, Washington, DC 20057; {sect}Research Institute of Molecular Pathology (IMP), A-1030 Vienna, Austria; ||Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara 630-0101, Japan

Monitoring Editor: John Cleveland

The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the Activator Protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal, therefore transgenic mice encoding a c-Jun gene flanked by lox P sites (c-junf/f) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun-/- cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun-/- cells. As c-Src is a critical component of pathways regulating proliferation, survival and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion.

{dagger}These authors contributed equally to this work.

Address correspondence to: Richard G. Pestell (Richard.Pestell{at}jefferson.edu)






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