Gastric Cancer
Copyright ©The Author(s) 2004.
World J Gastroenterol. Apr 15, 2004; 10(8): 1110-1114
Published online Apr 15, 2004. doi: 10.3748/wjg.v10.i8.1110
Figure 1
Figure 1 VES induced apoptosis by DNA fragmentation in SGC-7901 cells. Lane 1: Molecular weight marker; Lane 2: UT control; Lane 3: succinate; Lane 4: vitamin E; Lane 5: VES at 5 mg/L; Lane 6: VES at 10 mg/L; Lane 7: VES at 20 mg/L.
Figure 2
Figure 2 Expression of p-JNK and JNK in SGC-7901 cells follow-ing treatment of VES for 24 h. Lane 1: molecular weight marker; Lane 2: UT control; Lane 3: succinate; Lane 4: vitamin E; Lane 5: VES at 5 mg/L; Lane 6: VES at 10 mg/L; Lane 7: VES at 20 mg/L.
Figure 3
Figure 3 Expression of p-JNK and JNK in SGC-7901 cells fol-lowing treatment of VES at 20 mg/L at different time points. Lane 1: molecular weight marker; Lane 2: UT control; Lanes 3-7: 20 mg/L VES treatment for 1.5, 3, 6, 12, 24 h.
Figure 4
Figure 4 Effect of DN-JNK on VES-induced apoptosis. A: SGC-7901 cells were stained with DAPI; B: The apoptotic rate.
Figure 5
Figure 5 Effect of DN-JNK on expression of JNK and c-Jun when DN-JNK was transfected into SGC-7901 cells following treatment of VES for 24 h.