Small molecule inhibitors
|
Signal proteins inhibited
|
Amount used to treat cells
|
Cell elongation index
|
Preventive effect (%)
|
---|
Control
|
N/A
|
N/A
|
1.0 ± 0.24
|
None
|
MSP
|
none
|
2.0 nM
|
3.12 ± 0.47
|
N.D
|
CP-1
|
RON
|
100 μM
|
1.05 ± 0.26
|
98.4%
|
PD98059
|
MEK1/2
|
100 μM
|
1.03 ± 0.31
|
97.1%
|
Wortmannin
|
PI-3 kinase
|
50 μM
|
2.9 ± 0.41
|
7.1%
|
SB203580
|
p38 MAP kinase
|
50 μM
|
3.1 ± 4.6
|
0.6%
|
SP600125
|
JNK1,2,3
|
5 μM
|
3.07 ± 0.39
|
1.6%
|
Cay10512
|
NF-κB
|
5 μM
|
2.03 ± 0.33
|
39.4%
|
S31-201
|
Stat3
|
10 μM
|
1.25 ± 0.34
|
59.9%
|
XAV-939
|
Wnt/β-catenin
|
5 μM
|
2.16 ± 0.32
|
30.8%
|
SL0101
|
RSK
|
50 μM
|
1.09 ± 0.27
|
97.1%
|
Rapamycin
|
FRAP/mTOR
|
100 nM
|
2.69 ± 0.25
|
13.8%
|
Vismodegib
|
Hedgehog
|
1 μM
|
2.04 ± 0.22
|
34.6%
|
SB431542
|
TGF-β1 receptor
|
1 μM
|
2.97 ± 0.24
|
4.8%
|
- *M-RON cells (1 × 104 cells/well) in DMEM containing 1% FBS were stimulated with 2 nM of MSP in the presence of absence of individual small chemical inhibitors for 24 h. Cell morphological changes were observed under microscope and photographed with CCD camera. Cell elongation index (CEI) was determined by measuring the length of individual adherent cells among various groups. CEI from control cells was set as one. The percentages of preventive effect were calculated by comparing with as the CEI from MSP-treated cells previously described [45]