FOXC1 and cancer: The inhibition of the cell adhesion mediator E-cadherin by FOXC1 transactivation of E-cadherin's direct repressor, Snai1, as well as the overexpression FOXC1's direct transcriptional target, NEDD9, have been positively correlated with increased cancer cell migration and invasion [26, 27] and may be involved in the FOXC1 regulation of EMT.