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Published ahead of print on October 6, 2005, doi:10.1165/rcmb.2005-0130OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 2, February 2006, 142-150

A more recent version of this article appeared on February 1, 2006
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Submitted on April 10, 2005
Revised on October 4, 2005

Nuclear Factor-{kappa}B Affects Tumor Progression in a Mouse Model of Malignant Pleural Effusion

Georgios T Stathopoulos1*, Zhiwen Zhu2, M. Brett Everhart3, Ioannis Kalomenidis4, William E Lawson5, Semra Bilaceroglu6, Todd E Peterson7, Daphne Mitchell1, Fiona E Yull8, Richard W Light6, and Timothy S Blackwell9

1 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA, 2 Pulmonary Division, Saint Thomas Hospital, Nashville, TN, USA; Department of Pulmonary Medicine, 1st affiliated Hospital of Zhongshan (Sun Yat-sen) University, Guangzhou, Guangdong, China, 3 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA, 4 Department of Critical Care and Pulmonary Services, Evangelismos Hospital, University of Athens, School of Medicine, Athens, Attica, Greece, 5 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Veterans Affairs, VA Tennessee Valley Healthcare System, Nashville, TN, USA, 6 Pulmonary Division, Saint Thomas Hospital, Nashville, TN, USA, 7 Department of Radiology and Radiological Sciences, Vanderbilt Institute of Imaging Science, Nashville, TN, USA, 8 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA, 9 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Veterans Affairs, VA Tennessee Valley Healthcare System, Nashville, TN, USA

* To whom correspondence should be addressed. E-mail: georgios.stathopoulos{at}vanderbilt.edu.

We developed a novel mouse model of malignant pleural effusion (MPE) by injecting Lewis lung cancer (LLC) cells directly into the pleural space of syngeneic C57B/6 mice. The pleural effusions in this model share common cellular and biochemical features with human MPEs. Implantation and growth of pleural tumors triggers a host inflammatory response characterized by a mixed inflammatory cell influx into the pleural fluid. LLC cells exhibited high basal Nuclear Factor-{kappa}B (NF-{kappa}B) activity in vitro and in vivo, which we used to drive expression of a NF-{kappa}B-dependent green fluorescent protein-firefly luciferase fusion reporter construct. NF-{kappa}B-dependent reporter expression allowed intravital tracing of pleural tumors. Inhibition of NF-{kappa}B in LLC cells did not affect cell viability in culture; however, injection of LLC cells expressing a dominant NF-{kappa}B inhibitor resulted in decreased tumor burden, decreased pleural effusion volume, and decreased pleural effusion TNF-{alpha} levels. These studies indicate that tumor NF-{kappa}B activity regulates pleural tumor progression. This reproducible model of MPE can be used to further study the influence of specific host and tumor factors on the pathogenesis of MPE and evaluate new therapeutic strategies.




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