Skip to main content
. 2014 Dec 18;6(5):3123–3135. doi: 10.18632/oncotarget.3060

Figure 5. Slit2/Robo1 signaling activates the Src-mediated inhibition of E-cadherin.

Figure 5

IHC analysis of the expression of total Src and pSrc (Tyr416) in the tumor tissues of ApcMin/+ and ApcMin/+;Slit2 mice (A). Inactivation of Slit2/Robo1 significantly reduced the expression of pSrc (Tyr 416) in SW620 and SW480 cells, and activation of Slit2/Robo1 signaling through overexpressing Slit2 or Robo1 expression promotes pSrc (Tyr 416) expression in HCT-116 cells (B). IHC analysis of the expression of E-cadherin in the tumor tissues of the ApcMin/+ and ApcMin/+;Slit2 mice (C). Inactivation of Src signaling significantly enhances the expression of E-cadherin but inhibits the expression of β-cateninin in SW620 and SW480 cells (D). Src inactivation in SW620 and SW480 cells also led to a reduced nuclear translocation of β-catenin (E). Inhibition of E-cadherin expression through siRNA technique could promote the expression of β-cateninin and vimentin in SW620 and SW480 cells (F). IHC analysis of the expression of vimentin in the tumor tissues of ApcMin/+ and ApcMin/+;Slit2 mice (G). The data in IHC staining are representative of 11 mice per group (All mice were 24-week-old). The results of IHC were determined using IPP software, and the data were expressed as the mean ±S.D. *: P < 0.05, **: P < 0.01. Scale bars: 20 μm (A, C and G) and 25 μm (E).