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Papers In Press, published online ahead of print April 24, 2001
J. Biol. Chem, 10.1074/jbc.C100140200
Submitted on March 23, 2001
Revised on April 23, 2001
Accepted on April 23, 2001

Non-small cell lung cancer cyclooxygenase-2-dependent invasion is mediated by CD44

Mariam Dohadwala, Jie Luo, Li Zhu, Ying Lin, Graeme J. Dougherty, Sherven Sharma, Min Huang, Mehis Pold, Raj K. Batra, and Steven M. Dubinett

Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095-1690

Corresponding Author: sdubinett{at}mednet.ucla.edu

Summary Elevated tumor cyclooxygenase (COX-2) expression is associated with increased angiogenesis, tumor invasion and suppression of host immunity. We have previously shown that genetic inhibition of tumor COX-2 expression reverses the immunosuppression induced by non-small cell lung cancer (NSCLC). To assess the impact of COX-2 expression in lung cancer invasiveness, NSCLC cell lines were transduced with a retroviral vector expressing the human COX-2 cDNA in the sense (COX-2-S) and antisense (COX-2-AS) orientations. COX-2-S clones expressed significantly more COX-2 protein, produced 10 fold more PGE2 and demonstrated an enhanced invasive capacity compared to control vector-transduced or parental cells. CD44, the cell surface receptor for hyaluronate, was overexpressed in COX-2-S cells, and specific blockade of CD44 significantly decreased tumor cell invasion. In contrast, COX-2-AS clones had a very limited capacity for invasion and showed diminished expression of CD44. These findings suggest that a COX-2-mediated, CD44-dependent pathway is operative in NSCLC invasion. Because tumor COX-2 expression appears to have a multifaceted role in conferring the malignant phenotype, COX-2 may be an important target for gene or pharmacologic therapy in NSCLC.


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