Study of biological behavior of stromal cell-derived factor-1 on multiple myeloma cell migration and adhesion.
- Author:
Xiao-hui ZHANG
1
;
Jin-xiang FU
;
Jian-hua ZHANG
;
Yang-min ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Blotting, Western; Cell Adhesion; drug effects; physiology; Cell Adhesion Molecules; metabolism; Cell Line, Tumor; Cell Movement; drug effects; physiology; Chemokine CXCL12; pharmacology; physiology; Enzyme Activation; drug effects; Flow Cytometry; Fluorescent Antibody Technique; Humans; Integrin alpha4; metabolism; Integrin alpha5; metabolism; Integrin beta1; metabolism; Multiple Myeloma; metabolism; pathology; physiopathology; Phosphatidylinositol 3-Kinases; metabolism; Signal Transduction; drug effects; physiology
- From: Chinese Journal of Hematology 2006;27(4):240-243
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the biological behavior of stromal cell-derived factor-1 (SDF-1) on multiple myeloma (MM) cell migration and adhesion and it related signaling pathways.
METHODSExpression of adhesion molecules on MM cells of RPMI8226, XG-1 and XG-7 cells was analysed by flow cytometry, the influence of SDF-1 on CD29 and CD49e distribution by immunofluorescence, the effect of SDF-1 on chemotaxis of MM cells by transwell assay. Activation of phosphoinositide-3 kinase (PI3K) in MM cells treated with SDF-1 and by immunoblotting.
RESULTS3 strains of MM cell line expressed many adhesion molecule. RPMI8226, XG-7 cells were all high level of expression of CD29 (> 70%). XG-1, XG-7 cells were all high level of expression of CD44 (> 80%), and XG-7 cells was of CD49d (> 90%). In all of 3 strains, the levels of expression of CD49e were low (< 30%). SDF-1 could not upregulate their expression, but could trigger the establishment of polarized morphology of MM cells and the redistribution of CD29 and CD49e. SDF-1 promoted MM cells adhesion to endothelial cells, stimulated phosphorylation of P85 subunit of PI3K in MM cells and induced MM cells migration, which were inhibited by G protein inhibitor PTX and PI3K inhibitor wortmannin.
CONCLUSIONSDF-1 can promote MM cell adhesion to endothelial cells, trigger establishment of a polarized morphology of MM cells and redistribution of adhesion molecules and induce MM cells migration via PI3K signaling pathway.