Host nuclear factor-kappaB activation potentiates lung cancer metastasis.

Stathopoulos GT, Sherrill TP, Han W, Sadikot RT, Yull FE, Blackwell TS, Fingleton B
Mol Cancer Res. 2008 6 (3): 364-71

PMID: 18337446 · DOI:10.1158/1541-7786.MCR-07-0309

Epidemiologic and experimental evidence suggests that a link exists between inflammation and cancer, although this relationship has only recently begun to be elucidated for lung cancer, the most frequently fatal human tumor. Nuclear factor-kappaB (NF-kappaB), a transcription factor that controls innate immune responses in the lungs, has been implicated as an important determinant of cancer cell proliferative and metastatic potential; however, its role in lung tumorigenesis is uncertain. Here, we specifically examine the role of NF-kappaB-induced airway inflammation in lung cancer metastasis using a model of intravenous injection of Lewis lung carcinoma cells into immunocompetent C57Bl/6 mice. Induction of lung inflammation by direct and specific NF-kappaB activation in airway epithelial cells potentiates lung adenocarcinoma metastasis. Moreover, we identify resident lung macrophages as crucial effectors of lung susceptibility to metastatic cancer growth. We conclude that NF-kappaB activity in host tissue is a significant factor in the development of lung metastasis.

MeSH Terms (14)

Adenoviruses, Human Animals Cell Division Cell Line, Tumor Chemokine CCL2 Chemokine CCL8 Genes, Reporter Genetic Vectors Humans Lung Neoplasms Matrix Metalloproteinase 9 Neoplasm Metastasis NF-kappa B Tumor Necrosis Factor-alpha

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