1. Volume 41, Issue 2, Pages 267-273 (August 2004)
SU5416 is a potent inhibitor of hepatocyte growth factor receptor (c-Met) and blocks HGF-induced invasiveness of human HepG2 hepatoma cells 
Si Y. Wang, Bing Chen, Yi Q. Zhan, Wang X. Xu, Chang Y. Li, Ri F. Yang, Hong Zheng, Pei B. Yue, Steven H. Larsen, Hui B. Sun, Xiaoming Yang 
Journal of Hepatology 
Volume 41, Issue 2, Pages (August 2004)
DOI: /j.jhep

2. Fig. 1
Inhibition of cell motility by SU5416 in MDCK and HepG2 cells. Cells were plated in 24-well plates at a density of 1×104 cells/well and cultured for 24 h in the medium containing HGF (20 ng/ml) with or without 2 μM SU5416. The cells were fixed, stained with 0.2% crystal violet and photographed.
Journal of Hepatology  , DOI: ( /j.jhep )

3. Fig. 2
Effect of SU5416 on HGF-induced invasive activity in HepG2 cells. Invasive activity was determined by the invasiveness assay as described in Section 2. Five fields per well were selected for cell counts. Each sample was repeated with three wells and all experiments were independently performed in triplicate. Data shown is the mean±SD. **P<0.01 compared with control.
Journal of Hepatology  , DOI: ( /j.jhep )

4. Fig. 3
Effects of SU5416 on HGF-induced DNA synthesis in rat primary cultured hepatocytes and ECV304 vascular endothelial cells. (a) Rat parenchyma hepatocytes and ECV304 cells were cultured in the presence of various concentrations of HGF for 48 h, and the proliferation was detected by [3H]thymidine incorporation. (b) Rat parenchyma hepatocytes and ECV304 cells were cultured in the presence of 20 ng/ml HGF and various concentrations of SU5416 for 48 h, and pulse-labeled with [3H]thymidine for 3 h. Each value represents the mean±SD of triplicate measurements. *P<0.05, **P<0.01 compared with control.
Journal of Hepatology  , DOI: ( /j.jhep )

5. Fig. 4
Effect of SU5416 on HGF-induced c-Met receptor tyrosine phosphorylation. (a) Serum-starved rat cultured hepatocytes (left) or HepG2 cells (right) were pre-treated 2 h with or without various concentrations of SU5416, then cells were stimulated with 20 ng/ml HGF for 10 min. Cell lysates were immunoprecipitated with anti-c-Met antibody, and blotted with anti-p-Tyr antibody. (b) Effects of SU5416 on HGF-mediated signaling occurred even downstream of c-Met activation. Serum-starved rat cultured hepatocytes were pre-treated 2 h with or without various concentrations of SU5416, then cells were stimulated with 20 ng/ml HGF. Western blot analysis of ERK1/2, p-ERK, Akt and p-Akt were described in Section 2.
Journal of Hepatology  , DOI: ( /j.jhep )

6. Fig. 5
SU5416 reverses the phenotype of NIH3T3 cells transformed by Tpr-met. (a) A stable clone of transformed NIH3T3 and analogous control cells were lysed and analyzed by Western blotting. (b) The Tpr-met stably transfected cells were mixed with 1 ml top ultra pure agar (0.3%) with or without SU5416, and plated in triplicate on top of 1 ml bottom ultra pure agar (0.6%) in DMEM plus 20% FCS, G418 (400 mg/l), 100 U/ml penicillin and 80 μg/ml streptomycin at a density of 1×103 cells per 35-mm well. Colonies containing more than 50 cells were scored under the microscope after 2 weeks. **P<0.01 compared with control.
Journal of Hepatology  , DOI: ( /j.jhep )