NDLI: Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.

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Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Deng, Jiong Fujimoto, Junya Ye, Xiao-Feng Men, Tao-Yan Van Pelt, Carolyn S. Chen, Yu-Long Lin, Xiao-Feng Kadara, Humam Tao, Qingguo Lotan, Dafna Lotan, Reuben
Description	Country affiliation: United States Author Affiliation: Deng J ( Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.)
Abstract	Mouse models can be useful for increasing the understanding of lung tumorigenesis and assessing the potential of chemopreventive agents. We explored the role of inflammation in lung tumor development in mice with knockout of the tumor suppressor Gprc5a. Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a(-/-) mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice. Gprc5a(-/-) mouse lungs contained higher constitutive levels of proinflammatory cytokines and chemokines and were more sensitive than lungs of Gprc5a(+/+) mice to stimulation of NF-kappaB activation by lipopolysaccharide in vivo. Studies with epithelial cells cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-) adenocarcinoma cells by reexpression of Gprc5a. Compared with Gprc5a(+/+) cells, the Gprc5a(-/-) cells produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration. Silencing Gprc5a and the p65 subunit of NF-kappaB in Gprc5a(+/+) and Gprc5a(-/-) cells, respectively, reversed these effects. Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.
File Format	HTM / HTML
ISSN	19406207
e-ISSN	19406215
Journal	Cancer Prevention Research
Issue Number	4
Volume Number	3
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2010-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Oncology Adenocarcinoma Metabolism Cell Transformation, Neoplastic Lung Neoplasms Nf-kappa B Pneumonia Receptors, G-protein-coupled Genetics Immunology Animals Chemotaxis, Leukocyte Electrophoretic Mobility Shift Assay Enzyme Activation Immunoblotting Immunohistochemistry Macrophages Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Rna, Messenger Rna, Small Interfering Deficiency Respiratory Mucosa Pathology Reverse Transcriptase Polymerase Chain Reaction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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