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Am J Physiol Cell Physiol (December 14, 2005). doi:10.1152/ajpcell.00450.2005
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Submitted on September 6, 2005
Accepted on December 10, 2005

Induced focal adhesion kinase expression suppresses apoptosis by activating NF-{kappa}B signaling in intestinal epithelial cells

Huifang M Zhang1, Kaspar M Keledjian1, Jaladanki N Rao1, Tongtong Zou1, Lan Liu1, Bernard S Marasa2, Shelley R Wang3, Lisa Ru3, Eric D Strauch4, and Jian-Ying Wang5*

1 Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA; Research Service, Baltimore VA Medical Center, Baltimore, Maryland, USA
2 Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Research Service, Baltimore VA Medical Center, Baltimore, Maryland, USA
3 Research Service, Baltimore VA Medical Center, Baltimore, Maryland, USA
4 Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA
5 Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA; Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Research Service, Baltimore VA Medical Center, Baltimore, Maryland, USA

* To whom correspondence should be addressed. E-mail: jwang{at}smail.umaryland.edu.

Focal adhesion kinase (FAK) integrates various extracellular and intracellular signals and is implicated in a variety of biological functions, but its exact role and down-stream targeting signals in the regulation of apoptosis in intestinal epithelial cells remain unclear. The current study tested the hypothesis that FAK has an antiapoptotic role in intestinal epithelial cells (IEC-6 line) by altering NF-{kappa}B signaling. Induced FAK expression by stable transfection with the wild-type (WT) FAK gene increased FAK phosphorylation, which was associated with an increase in NF-{kappa}B activity. These stable WT-FAK-transfected IEC cells also exhibited an increased resistance to apoptosis when they were exposed to tumor necrosis factor-{alpha} plus cycloheximide (TNF-{alpha}/CHX). Specific inhibition of NF-{kappa}B by the recombinant adenoviral vector containing I{kappa}B{alpha} superrepressor prevented the increased resistance to apoptosis in WT-FAK-transfected cells. In contrast, inactivation of FAK by ectopic expression of dominant negative mutant of FAK (DNM-FAK) inhibited NF-{kappa}B activity and increased the sensitivity to TNF-{alpha}/CHX-induced apoptosis. Furthermore, induced expression of endogenous FAK by depletion of cellular polyamines also increased NF-{kappa}B activity and resulted in the increased resistance to TNF-{alpha}/CHX-induced apoptosis, which were prevented by overexpression of DNM-FAK. These results indicate that increased expression of FAK suppresses TNF-{alpha}/CHX-induced apoptosis, at least partially, through activation of NF-{kappa}B signaling in intestinal epithelial cells.




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