Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor.

Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Research Abstract Details 

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Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Abstract Text:

Beatriz E Rendon,Thierry Roger,Ivo Teneng,Ming Zhao,Yousef Al-Abed,Thierry Calandra,Robert A Mitchell,Beatriz E Rendon,Thierry Roger,Ivo Teneng,Ming Zhao,Yousef Al-Abed,Thierry Calandra,Robert A Mitchell,

Macrophage migration inhibitory factor (MIF) is expressed and secreted in response to mitogens and integrin-dependent cell adhesion. Once released, autocrine MIF promotes the activation of RhoA GTPase leading to cell cycle progression in rodent fibroblasts. We now report that small interfering RNA-mediated knockdown of MIF and MIF small molecule antagonism results in a greater than 90% loss of both the migratory and invasive potential of human lung adenocarcinoma cells. Correlating with these phenotypes is a substantial reduction in steady state as well as serum-induced effector binding activity of the Rho GTPase family member, Rac1, in MIF-deficient cells. Conversely, MIF overexpression by adenovirus in human lung adenocarcinoma cells induces a dramatic enhancement of cell migration, and co-expression of a dominant interfering mutant of Rac1 (Rac1(N17)) completely abrogates this effect. Finally, our results indicate that MIF depletion results in defective partitioning of Rac1 to caveolin-containing membrane microdomains, raising the possibility that MIF promotes Rac1 activity and subsequent tumor cell motility through lipid raft stabilization.

Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Publishing Authors By Initials

BE Rendon,T Roger,I Teneng,M Zhao,Y Al-Abed,T Calandra,RA Mitchell,BE Rendon,T Roger,I Teneng,M Zhao,Y Al-Abed,T Calandra,RA Mitchell,

For similar enzymes and coenzymes: enzymes: hydrolases: acid anhydride hydrolases: gtp phosphohydrolases: gtp-binding proteins: monomeric gtp-binding proteins: rho gtp-binding proteins: rhoa gtp-binding protein research abstracts see: enzymes and coenzymes: enzymes: hydrolases: acid anhydride hydrolases: gtp phosphohydrolases: gtp-binding proteins: monomeric gtp-binding proteins: rho gtp-binding proteins: rhoa gtp-binding protein research

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Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 29910-8

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 20

MONTH: 08

YEAR: 2007

Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Keywords Mesh Terms:

KEYWORDS: rhoA GTP-Binding Protein

MESH TERMS: metabolism

Chemical & Substance for Abstract: Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor. Information

Substance Name: rhoA GTP-Binding Protein

Registry Number: EC 3.6.5.2

Grant and Affiliation Information for Regulation of human lung adenocarcinoma cell migration and invasion by macrophage migration inhibitory factor.

AFFILIATION: Molecular Targets Program, J. G. Brown Cancer Center, University of Louisville, Louisville, Kentucky 40202, USA.

Country: United States

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MEDLINETA: J Biol Chem

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