期刊
VETERINARY PATHOLOGY
卷 50, 期 5, 页码 895-902出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0300985813476061
关键词
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; animal model; lipopolysaccharide; lung tumor; macrophage
资金
- NIH [8K01OD010970]
- Masonic Cancer Center and College of Veterinary Medicine, University of Minnesota
The association between pulmonary inflammation and lung cancer is well established. However, currently there are no appropriate models that recapitulate inflammation-related lung cancer in humans. In the present study, we examined, in 2 tumor bioassays, enhancement by bacterial lipopolysaccharide (LPS) of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice. Mice that were treated with NNK alone developed 29.6 +/- 9.8 and 36.2 +/- 4.1 lung tumors per mouse in experiments 1 and 2, respectively. Chronic intranasal instillation of LPS to NNK-treated mice increased the multiplicity of lung tumors to 47.3 +/- 16.1 and 51.2 +/- 4.8 lung tumors per mouse in experiments 1 and 2, corresponding to a significant increase by 60% and 41%, respectively. Moreover, administration of LPS to NNK-pretreated mice significantly increased the multiplicity of larger tumors and histopathologically more advanced lesions (adenoma with dysplasia and adenocarcinoma), macrophage recruitment to the peritumoral area, and expression of inflammation-, cell proliferation-, and survival-related proteins. Overall, our findings demonstrated the promise of the NNK-LPS-A/J mice model to better understand inflammation-driven lung cancer, dissect the molecular pathways involved, and identify more effective preventive and therapeutic agents against lung cancer.
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