Abstract:
:We used an experimental murine cancer metastasis model in which a colon adenocarcinoma cell line generates lung metastases, whose growth is stimulated in response to injection of bacterial lipopolysaccharide (LPS), to investigate the role of NF-kappaB in inflammation-induced tumor growth. We found that LPS-induced metastatic growth response in this model depends on both TNFalpha production by host hematopoietic cells and NF-kappaB activation in tumor cells. Inhibition of NF-kappaB in both colon and mammary carcinoma cells converts the LPS-induced growth response to LPS-induced tumor regression. The latter response is TNFalpha-independent, but depends on another member of the TNF superfamily, TRAIL, whose receptor is induced in NF-kappaB-deficient cancer cells.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Luo JL,Maeda S,Hsu LC,Yagita H,Karin Mdoi
10.1016/j.ccr.2004.08.012keywords:
subject
Has Abstractpub_date
2004-09-01 00:00:00pages
297-305issue
3eissn
1535-6108issn
1878-3686pii
S153561080400217Xjournal_volume
6pub_type
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