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1998 ; 89
(5
): 571-7
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Intracellular Signal-transducing elements involved in transendothelial migration
of lymphoma cells
#MMPMID9685862
Tsuzuki S
; Toyama-Sorimachi N
; Kitamura F
; Tsuboi H
; Ando J
; Sakurai T
; Morii N
; Narumiya S
; Miyasaka M
Jpn J Cancer Res
1998[May]; 89
(5
): 571-7
PMID9685862
show ga
To investigate the molecular mechanisms underlying transendothelial migration of
tumor cells, an essential process for their hematogenous dissemination, we
developed an in vitro model system that allows the separate monitoring of cell
adhesion and transmigration processes. This system uses a human pre-B lymphoma
cell line, Nalm-6, and a cultured mouse endothelial cell line, KOP2.16. Nalm-6
cells rapidly adhered to KOP2.16 and subsequently transmigrated underneath them.
Using this model, we examined the effects on transendothelial migration, of
various reagents which specifically interfere with the function of intracellular
signal transduction molecules. Treatment of Nalm-6 cells with wortmannin (WMN),
herbimycin A, pertussis toxin, or C3 exoenzyme of Clostridium botulinum, which
specifically inhibit P13 kinase and/or myosin light chain kinase,
herbimycin-sensitive tyrosine kinases, heterotrimeric G proteins, and the small G
proteins, and the small G proteins rho/rac, respectively, reduced transmigration
in a dose-dependent manner, Pretreatment of KOP2.16 endothelial cells with WMN
also reduced transmigration in a dose-dependent manner. Binding of Nalm-6 binding
to KOp2.16 was not affected, even when Nalm-6 or KOP2.16 cells were pretreated
with these inhibitors, indicating that the reduction of transmigration was not
due to a reduction of Nalm-6 to KOP2.16. These results also indicate that the
signal transduction pathway(s) involved in transmigration can be dissociated from
that of adhesion. Our results support the notion that endothelial cells are not a
passive barrier in lymphoma extravasation, but that they assist lymphoma cell
extravasation.
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