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A more recent version of this article appeared on April 14, 2006
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M513008200v1
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Papers In Press, published online ahead of print February 20, 2006
J. Biol. Chem, 10.1074/jbc.M513008200
Submitted on December 6, 2005
Revised on January 27, 2006
Accepted on February 20, 2006

A phosphatidylinositol 3-kinase regulated Akt independent signaling promotes cigarette smoke induced FRA-1 expression

Qin Zhang, Pavan Adiseshaiah, Dhananjaya V. Kalvakolanu, and Sekhar P. Reddy

Enviromental Health Sciences, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD 21205

Corresponding Author: sreddy{at}jhsph.edu

The FRA-1 protooncogene is overexpressed in a variety of human tumors and is known to upregulate the expression of genes involved in tumor progression and invasion. The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is also to known regulate these cellular processes. More importantly, respiratory toxicants and carcinogens activate both the PI3K-Akt pathway and FRA-1 expression in human bronchial epithelial (HBE) cells. In this report we investigated a potential link between the PI3K-Akt pathway and the CS-stimulated epidermal growth factor receptor (EGFR)-mediated FRA-1 induction in non-oncogenic HBE cells. Treatment of cells with LY294002, an inhibitor of the PI3K-Akt pathway, completely blocked CS-induced FRA-1 expression. Surprisingly, pharmacological inhibition of Akt had no significant effect on CS-induced FRA-1 expression. Likewise, the inhibition of PKCzeta , which is known downstream effector of PI3K, did not alter FRA-1 expression. We found that the PI3K through p21-activated kinase 1 (PAK1) regulates FRA-1 proto-oncogene induction by CS and the subsequent activation of the Elk1 and CREB transcription factors that are bound to the promoter in HBE cells.


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