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Published ahead of print on March 3, 2005, doi:10.1165/rcmb.2004-0223OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 32, pp. 540-547, 2005
© 2005 American Thoracic Society
DOI: 10.1165/rcmb.2004-0223OC

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

Pei-Li Yao, Yi-Chen Lin, Chien-Hsun Wang, Ya-Chen Huang, Wei-Yu Liao, Shan-Shue Wang, Jeremy J. W. Chen* and Pan-Chyr Yang*

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

Correspondence and requests for reprints should be addressed to Pan-Chyr Yang, M.D., Ph.D., Department of Internal Medicine, National Taiwan University Hospital, No. 7, Chung-Shan South Rd, Taipei, Taiwan 100, R.O.C. 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 phorbol myristate acetate–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 tumor necrosis factor (TNF)-{alpha} and IL-1{alpha} could induce IL-8 expression in lung cancer cells in a dose-dependent manner. Neutralization with TNF-{alpha} and IL-1{alpha} antibodies in cocultures decreased the levels of IL-8 expression in sensitized lung cancer cells. Nuclear factor-{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 nuclear factor-{kappa}B pathway and modulated by TNF-{alpha} and IL-1{alpha}.

Key Words: autocrine • inflammation • lung cancer • macrophages • NF-{kappa}B




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