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J. Biol. Chem., Vol. 276, Issue 36, 33762-33772, September 7, 2001
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From Adhesion and migration of tumor cells on and
through the vascular endothelium are critical steps of the metastatic
invasion. We investigated the roles of E-selectin and of
stress-activated protein kinase-2 (SAPK2/p38) in modulating endothelial
adhesion and transendothelial migration of HT-29 colon carcinoma cells. Tumor necrosis factor
Transendothelial Migration of Colon Carcinoma Cells
Requires Expression of E-selectin by Endothelial Cells and Activation
of Stress-activated Protein Kinase-2 (SAPK2/p38) in the Tumor
Cells*
§,,
Le Centre de Recherche en Cancérologie de
l'Université Laval, L'Hôtel-Dieu de Québec,
Québec G1R-2J6, Canada and the ¶ Department of Radiation
Oncology, Massey Cancer Center, Virginia Commonwealth University,
Richmond, Virginia 23298-0058
(TNF) strongly increased the expression of
E-selectin in human umbilical vein endothelial cells (HUVEC). This
effect was independent of the activation of SAPK2/p38 induced by
TNF. Adhesion of HT-29 cells on a monolayer of HUVEC pretreated with
TNF was dependent on E-selectin expression but was independent of
SAPK2/p38 activity of both HUVEC and tumor cells. The adhesion of HT-29
cells to E-selectin-expressing HUVEC led to the activation of SAPK2/p38
in the tumor cells as reflected by the increased phosphorylation of the
actin-polymerizing factor HSP27 by mitogen-activated protein kinase
2/3, a direct target of SAPK2/p38. Moreover, a recombinant
E-selectin/Fc chimera quickly increased the activation of SAPK2/p38 in
HT-29 cells. Blocking the increased activity of SAPK2/p38 of HT-29
cells by SB203580 or by expressing a dominant negative form of
SAPK2/p38 inhibited their transendothelial migration. Similarly, HeLa
cells stably expressing a kinase-inactive mutant of SAPK2/p38 showed a
decreased capacity to cross a layer of HUVEC. Overall, our results
suggest that the regulation of transendothelial migration of tumor
cells involves two essential steps as follows: adhesion to the
endothelium through adhesion molecules, such as E-selectin, and
increased motogenic potential through adhesion-mediated activation of the SAPK2/p38 pathway.
*
This work was supported by Canadian Institutes of Health
Research Grant MT15402, the Cancer Research Society Inc., and United States Public Health Grant PHS CA53199.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Centre de
Recherche en Cancérologie de l'Université Laval,
L'Hôtel-Dieu de Québec, 11 Côte du Palais,
Québec, G1R 2J6, Canada. Tel.: 418-691-5553; Fax: 418-691-5439;
E-mail: Jacques.Huot@phc.ulaval.ca.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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