Regulation of the Metastatic Process by E-Selectin and Stress-Activated Protein Kinase-2/p38

: The formation of metastasis is a dreadful complication of cancer that is associated with a poor prognosis. Several clinical observations and experimental findings indicate that the metastatic process is nonrandom and involves a sequence of multistep events that may all be targeted for therapy. Thi...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2002-11, Vol.973 (1), p.562-572
Main Authors: LAFERRIÈRE, JULIE, HOULE, FRANÇOIS, HUOT, JACQUES
Format: Article
Language:English
Subjects:
adhesive molecules
breast cancer
Cell Adhesion - physiology
colon cancer
E-selectin
E-Selectin - physiology
endothelial cells
Endothelium, Vascular - physiopathology
Humans
integrins
liver metastasis
MAPK
metastasis
migration
Mitogen-Activated Protein Kinases - physiology
Models, Biological
Neoplasm Metastasis - physiopathology
p38 Mitogen-Activated Protein Kinases
SAPK2/p38
selectins
Signal Transduction
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Summary:: The formation of metastasis is a dreadful complication of cancer that is associated with a poor prognosis. Several clinical observations and experimental findings indicate that the metastatic process is nonrandom and involves a sequence of multistep events that may all be targeted for therapy. This includes angiogenesis of the primary neoplasm, release of malignant cells from this neoplasm, entry of cancer cells into the blood circulation, interaction of cancer cells with vascular endothelial cells in distant organs, and growth of blood‐borne cancer cells locally in the vessels or distally following extravasation. Our working hypothesis is that metastatic cancer cells exploit the mechanisms of the inflammation process to successfully migrate into distant organs. This implies a pivotal role for specific adhesive interactions between cancer cells and vascular endothelial cells and activation of migratory pathways in the cancer cells. We review here the roles played by the endothelial adhesive molecule E‐selectin and by the motogenic stress‐activated protein kinase‐2 (SAPK2/p38) pathway of cancer cells in modulating transendothelial migration of cancer cells.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2002.tb04702.x