Colorectal Cancer
Copyright ©2008 The WJG Press and Baishideng.
World J Gastroenterol. Jan 21, 2008; 14(3): 428-434
Published online Jan 21, 2008. doi: 10.3748/wjg.14.428
Figure 1
Figure 1 A: Expression of STAT3 protein in HT29 cells; B: STAT3 DNA-binding activity by EMSA in HT29 cells. 1: Control; 2, 3, 4: siRNA 2, 4, 8 nmol/L.
Figure 2
Figure 2 Effects of STAT3 siRNA on anchorage-independent growth of HT29 cells. It shows that treatment with STAT3 siRNA inhibit anchorage-independent growth in a dose-dependent manner. aP < 0.05 between siRNA 8 nmol/L and control groups.
Figure 3
Figure 3 Effects of STAT3 suppression on the invasion ability of HT29 cells.
Figure 4
Figure 4 Effects of STAT3 siRNA on anoikis of human colon cancer cell line HT29. A: AI (Apoptosis index) induced with STAT3 siRNA in HT29 cells; B: DNA ladder by STAT3 siRNA in HT29 cells. 1: Control; 2, 3, 4: siRNA, 2, 4, 8 nmol/L.
Figure 5
Figure 5 Knockdown of STAT3 expression downregulates Bcl-xL and survivin protein level in the HT29 human colon cancer cell line. A: Inhibition of transfection with STAT3 siRNA on Bcl-xL expression of colon cancer HT29 cell; B: Suppression of transfection with STAT3 siRNA on survivin expression of colon cancer HT29 cell.