Loss of Function of E-Cadherin in Embryonic Stem Cells and the Relevance to Models of Tumorigenesis

Figure 5

Fgf2 and Activin/Nodal signal transduction in mouse E-cadherin^−/− ES cells. (a) E-cadherin^−/− ES cells maintain pluripotency via Activin/Nodal signalling and self-renewal through Fgf2 signalling. (b) Wild-type ES cells treated with the FGFR1 small molecule inhibitor SU5402 exhibit similar proliferation rates compared to control-treated (DMSO) cells. (c) E-cadherin^−/− ES cells treated with the FGFR1 small molecule inhibitor SU5402 exhibit significantly reduced proliferation rates compared to control-treated (DMSO) cells.