Endotoxin/lipopolysaccharide activates NF-kappa B and enhances tumor cell adhesion and invasion through a beta 1 integrin-dependent mechanism.

Hdl Handle:
http://hdl.handle.net/10147/209012
Title:
Endotoxin/lipopolysaccharide activates NF-kappa B and enhances tumor cell adhesion and invasion through a beta 1 integrin-dependent mechanism.
Authors:
Wang, Jiang Huai; Manning, Brian J; Wu, Qiong Di; Blankson, Siobhan; Bouchier-Hayes, D; Redmond, H Paul
Affiliation:
Department of Academic Surgery, National University of Ireland, Cork University, Hospital, Ireland. jh.wang@ucc.i.e
Citation:
J Immunol. 2003 Jan 15;170(2):795-804.
Journal:
Journal of immunology (Baltimore, Md. : 1950)
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209012
PubMed ID:
12517943
Abstract:
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-kappaB activation in both SW480 and SW620 cells. Inhibition of the NF-kappaB 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-kappaB, 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.
Language:
eng
MeSH:
Adjuvants, Immunologic/*pharmacology; Antigens, CD14/biosynthesis/metabolism/pharmacology; Antigens, CD29/biosynthesis/*physiology; Cell Adhesion/immunology; Cell Membrane/immunology/metabolism; Cell Movement/*immunology; Endotoxins/*pharmacology; Humans; I-kappa B Proteins/genetics; Integrin alphaVbeta3/biosynthesis; Lipopolysaccharides/*pharmacology; NF-kappa B/antagonists & inhibitors/*metabolism; Peptides/pharmacology; Signal Transduction/immunology; Solubility; Transfection; Tumor Cells, Cultured/immunology/metabolism/*pathology; Up-Regulation/immunology
ISSN:
0022-1767 (Print); 0022-1767 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorWang, Jiang Huaien_GB
dc.contributor.authorManning, Brian Jen_GB
dc.contributor.authorWu, Qiong Dien_GB
dc.contributor.authorBlankson, Siobhanen_GB
dc.contributor.authorBouchier-Hayes, Den_GB
dc.contributor.authorRedmond, H Paulen_GB
dc.date.accessioned2012-02-03T15:09:53Z-
dc.date.available2012-02-03T15:09:53Z-
dc.date.issued2012-02-03T15:09:53Z-
dc.identifier.citationJ Immunol. 2003 Jan 15;170(2):795-804.en_GB
dc.identifier.issn0022-1767 (Print)en_GB
dc.identifier.issn0022-1767 (Linking)en_GB
dc.identifier.pmid12517943en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209012-
dc.description.abstractBeta(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-kappaB activation in both SW480 and SW620 cells. Inhibition of the NF-kappaB 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-kappaB, 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAdjuvants, Immunologic/*pharmacologyen_GB
dc.subject.meshAntigens, CD14/biosynthesis/metabolism/pharmacologyen_GB
dc.subject.meshAntigens, CD29/biosynthesis/*physiologyen_GB
dc.subject.meshCell Adhesion/immunologyen_GB
dc.subject.meshCell Membrane/immunology/metabolismen_GB
dc.subject.meshCell Movement/*immunologyen_GB
dc.subject.meshEndotoxins/*pharmacologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshI-kappa B Proteins/geneticsen_GB
dc.subject.meshIntegrin alphaVbeta3/biosynthesisen_GB
dc.subject.meshLipopolysaccharides/*pharmacologyen_GB
dc.subject.meshNF-kappa B/antagonists & inhibitors/*metabolismen_GB
dc.subject.meshPeptides/pharmacologyen_GB
dc.subject.meshSignal Transduction/immunologyen_GB
dc.subject.meshSolubilityen_GB
dc.subject.meshTransfectionen_GB
dc.subject.meshTumor Cells, Cultured/immunology/metabolism/*pathologyen_GB
dc.subject.meshUp-Regulation/immunologyen_GB
dc.titleEndotoxin/lipopolysaccharide activates NF-kappa B and enhances tumor cell adhesion and invasion through a beta 1 integrin-dependent mechanism.en_GB
dc.contributor.departmentDepartment of Academic Surgery, National University of Ireland, Cork University, Hospital, Ireland. jh.wang@ucc.i.een_GB
dc.identifier.journalJournal of immunology (Baltimore, Md. : 1950)en_GB
dc.description.provinceMunster-
All Items in Lenus, The Irish Health Repository are protected by copyright, with all rights reserved, unless otherwise indicated.