Skip to main content
. 2016 Jun 7;7(29):45060–45078. doi: 10.18632/oncotarget.9911

Figure 10. Scheme showing the interplay between C3G, p38α and Rap1 to regulate cell migration, invasion and tumor growth of HCT116 cells.

Figure 10

Upper panel, the diagram shows that C3G inhibits cell migration and invasion through down-regulation of p38α activity, either by preventing Rap1-mediated p38α activation by other Rap1GEFs or through p38α inhibition by alternative mechanisms. p38α promotes these processes. Changes in E-cadherin and ZO-1 expression and their cellular internalization, together with F-actin remodeling would mediate C3G/p38α actions on migration and invasion. MMP2 and MMP9 contribute to p38α induced invasion. Lower panel, the diagram shows that C3G and p38α promote tumor growth probably through independent pathways, inducing cell survival. Additionally, C3G through activation of cell adhesion may favor tumor growth. Rap1 inhibits tumor growth mainly through p38α independent mechanisms, although Rap1-mediated p38α activation could also prevent tumor growth by decreasing cell adhesion.