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Hepatocyte growth factor/scatter factor promotes adhesion of lymphoma cells
to extracellular matrix molecules via alpha 4 beta 1 and alpha 5 beta 1
integrins
IS Weimar, D de Jong, EJ Muller, T Nakamura, JM van Gorp, GC de Gast and WR Gerritsen
Department of Immunology, Netherlands Cancer Institute, Amsterdam.
Hepatocyte growth factor (HGF)/scatter factor (SF) is the ligand for a
tyrosine kinase cell surface receptor encoded by the MET protooncogene
(c-MET). HGF/SF can induce proliferation and motility in epithelial cells
and promotes invasion of carcinoma cells and NIH3T3 fibroblasts transfected
with both HGF/SF and c-MET genes. Our results show that HGF/ SF and c-MET
also play a role in adhesion and invasion of human lymphoma cells. c-MET
mRNA is expressed in hemopoietic cells, such as hemopoietic progenitor
cells (CD34+ cells) in bone marrow (BM) and mobilized peripheral blood,
immature B cells in cord blood and BM, and germinal center B-centroblasts.
In normal peripheral blood B cells, which are c-MET-, c-MET expression was
induced by PMA, ConA, HGF/ SF, and Epstein-Barr virus (EBV) infection.
Using immunohistochemistry, we detected c-MET on the cell surface of large
activated centroblasts in lymph nodes from patients with B-non-Hodgkin's
lymphoma and Hodgkin's disease. In the latter group, c-MET expression
correlated well with the presence of EBV. Because HGF/SF and c-MET promote
metastasis of carcinoma cells, we studied the effects of c-MET stimulation
by HGF/SF of B-lymphoma cells on properties relevant for metastasis, ie,
adhesion, migration, and invasion. HGF/SF stimulated adhesion of the c-
MET+ B-cell lines to the extracellular matrix molecules fibronectin (FN)
and collagen (CN) in a dose dependent manner. However, adhesion to laminin
was not affected by HGF/SF. Adhesion to FN was mediated by beta 1-integrins
alpha 4 beta 1 (VLA4) and alpha 5 beta 1 (VLA5) since blocking antibodies
against beta 1- (CD29), alpha 4-(CD49d), or alpha 5- (CD49e) integrin
subunits, completely reversed the effect of HGF/SF. Furthermore, HGF/SF
induced adhesion was abrogated by addition of genistein, which blocks
protein tyrosine kinases, including c-MET. Addition of HGF/SF resulted in a
sixfold increase in migration of c-MET B-lymphoma cells through Matrigel,
compared to medium alone. In rat fibroblast cultures, HGF/SF doubled the
number of c-MET+ B-lymphoma cells that invaded the fibroblast monolayer. In
these adhesion, migration and invasion assays HGF/SF had no effect on
c-MET- cell lines. In conclusion, c-MET is expressed or can be induced on
immature, activated, and certain malignant B cells. HGF/SF increased
adhesion of c-MET+ B-lymphoma cells to FN and CN, mediated via beta
1-integrins alpha 4 beta 1 and alpha 5 beta 1, and furthermore promoted
migration and invasion.
Volume 89,
Issue 3,
pp. 990-991000,
02/01/1997
Copyright © 1997 by The American Society of Hematology
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