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The Journal of Immunology, 2003, 170: 795-804.
Copyright © 2003 by The American Association of Immunologists

Endotoxin/Lipopolysaccharide Activates NF-{kappa}B and Enhances Tumor Cell Adhesion and Invasion Through a {beta}1 Integrin-Dependent Mechanism

Jiang Huai Wang1,*, Brian J. Manning*, Qiong Di Wu*, Siobhan Blankson*, D. Bouchier-Hayes{dagger} and H. Paul Redmond*

* Department of Academic Surgery, National University of Ireland, Cork University Hospital, Cork, Ireland; and {dagger} Department of Academic Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland

{beta}1 integrins play a crucial role in supporting tumor cell attachment to and invasion into the extracellular matrix. Endotoxin/LPS introduced by surgery has been shown to enhance tumor metastasis in a murine model. Here we show the direct effect of LPS on tumor cell adhesion and invasion in extracellular matrix proteins through a {beta}1 integrin-dependent pathway. The human colorectal tumor cell lines SW480 and SW620 constitutively expressed high levels of the {beta}1 subunit, whereas various low levels of {alpha}1, {alpha}2, {alpha}4, and {alpha}6 expression were detected. SW480 and SW620 did not express membrane-bound CD14; however, LPS in the presence of soluble CD14 (sCD14) significantly up-regulated {beta}1 integrin expression; enhanced tumor cell attachment to fibronectin, collagen I, and laminin; and strongly promoted tumor cell invasion through the Matrigel. Anti-{beta}1 blocking mAbs (4B4 and 6S6) abrogated LPS- plus sCD14-induced tumor cell adhesion and invasion. Furthermore, LPS, when combined with sCD14, resulted in NF-{kappa}B activation in both SW480 and SW620 cells. Inhibition of the NF-{kappa}B pathway significantly attenuated LPS-induced up-regulation of {beta}1 integrin expression and prevented tumor cell adhesion and invasion. These results provide direct evidence that although SW480 and SW620 cells do not express membrane-bound CD14, LPS in the presence of sCD14 can activate NF-{kappa}B, up-regulate {beta}1 integrin expression, and subsequently promote tumor cell adhesion and invasion. Moreover, LPS-induced tumor cell attachment to and invasion through extracellular matrix proteins is {beta}1 subunit-dependent.




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