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Published ahead of print on March 3, 2005, doi:10.1165/rcmb.2004-0223OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 6, June 2005, 540-547

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Submitted on July 16, 2004
Revised on July 14, 2004

Autocrine and Paracrine Regulation of IL-8 Expression in Lung Cancer Cells

Pei-Li Yao1, Yi-Chen Lin1, Chien- Hsun Wang2, Ya-Chen Huang2, Wei-Yu Liao3, Shan-Shue Wang4, Jeremy J.W. Chen5, and Pan-Chyr Yang6*

1 Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan; NTU Center for Genomic Medicine, National Taiwan University College of Medicine, Taipei, Taiwan, 2 Institutes of Biomedical Sciences and Molecular Biology, National Chung Hsing University, Taichung, Taiwan, 3 Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, 4 Department of Biochemical Engineering, Kao Yuan Institute of Technology, Kaohsiung, Taiwan, 5 NTU Center for Genomic Medicine, National Taiwan University College of Medicine, Taipei, Taiwan; Institutes of Biomedical Sciences and Molecular Biology, National Chung Hsing University, Taichung, Taiwan, 6 Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan; NTU Center for Genomic Medicine, National Taiwan University College of Medicine, Taipei, Taiwan; Academia Sinica, Institute of Biomedical Sciences, Taipei, Taiwan

* To whom correspondence should be addressed. E-mail: pcyang{at}ha.mc.ntu.edu.tw.

We had previously demonstrated that lung cancer cells, upon contact with macrophages, could be induced to secrete angiogenic factors to promote tumor angiogenesis. In this study, we focused on the paracrine and autocrine regulation of interleukin (IL)-8 expression in sensitized lung cancer cells after interacting with macrophages. We found that the IL-8 mRNA expression in lung cancer cells significantly increased after coculture with PMA-treated THP-1 cells and human primary lung macrophages. Fresh lung cancer CL1-5 cells cocultured with macrophage-sensitized lung cancer cells still had a 35% of increase in IL-8 mRNA expression. The addition of anti-inflammatory agents, pyrrolidine dithiocarbamate, pentoxifylline, aspirin and dexamethasone, could completely suppress the expression of IL-8 mRNA in fresh/sensitized lung cancer cell cocultures. Human recombinant TNF-{alpha} and IL1-{alpha} could induce IL-8 expression in lung cancer cells with dose-dependent manner. Neutralization with TNF-{alpha} and IL1-{alpha} antibodies in cocultures decreased the levels of IL-8 expression in sensitized lung cancer cells. Nuclear factor-{kappa}B (NF-{kappa}B) transcriptional activity was also suppressed by the same antibodies, as confirmed by a reporter gene assay and the electrophoretic mobility shift assay. Our results highly suggest that both autocrine and paracrine regulation are involved in IL-8 expression of lung cancer cells cocultured with macrophage. Also, the regulations of IL-8 expression in lung cancer cells were through the NF-{kappa}B pathway and modulated by TNF-{alpha} and IL1-{alpha}.




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