Inhibition of NF-kappaB in cancer cells converts inflammation- induced tumor growth mediated by TNFalpha to TRAIL-mediated tumor regression.

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 Cell

journal_title

Cancer cell

authors

Luo JL,Maeda S,Hsu LC,Yagita H,Karin M

doi

10.1016/j.ccr.2004.08.012

keywords:

subject

Has Abstract

pub_date

2004-09-01 00:00:00

pages

297-305

issue

3

eissn

1535-6108

issn

1878-3686

pii

S153561080400217X

journal_volume

6

pub_type

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