Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention
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[Cancer Research 64, 1853-1860, March 1, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Cyclooxygenase-2-Dependent Expression of Angiogenic CXC Chemokines ENA-78/CXC Ligand (CXCL) 5 and Interleukin-8/CXCL8 in Human Non-Small Cell Lung Cancer

Mehis Põld1,2, Li X. Zhu1,3, Sherven Sharma2,3, Marie D. Burdick1, Ying Lin1, Peter P. N. Lee1, Anu Põld1, Jie Luo1, Kostyantyn Krysan1,2, Mariam Dohadwala1,2, Jenny T. Mao1,2, Raj K. Batra2,3, Robert M. Strieter1,2 and Steven M. Dubinett1,2,3

1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, and 2 Lung Cancer Research Program, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, California, and 3 Veterans Affairs Greater Los Angeles Healthcare Center, Los Angeles, California

Elevated tumor cyclooxygenase (COX)-2 activity plays a multifaceted role in non-small cell lung cancer (NSCLC). To elucidate the role of COX-2 in the in vitro and in vivo expression of two known NSCLC angiogenic peptides, CXC ligand (CXCL) 8 and CXCL5, we studied two COX-2 gene-modified NSCLC cell lines, A549 and H157. COX-2 overexpression enhanced the in vitro expression of both CXCL8 and CXCL5. In contrast, specific COX-2 inhibition decreased the production of both peptides as well as nuclear translocation of nuclear factor {kappa}B. In a severe combined immunodeficient mouse model of human NSCLC, the enhanced tumor growth of COX-2-overexpressing tumors was inhibited by neutralizing anti-CXCL5 and anti-CXCL8 antisera. We conclude that COX-2 contributes to the progression of NSCLC tumorigenesis by enhancing the expression of angiogenic chemokines CXCL8 and CXCL5.




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Copyright © 2004 by the American Association for Cancer Research.