Globally, sE-cad protein expression levels increased in the all tested experimental systems, sE-cad contributed via HER family members to enhance MAPK, PI3K/Akt/mTOR, and IAP signaling, it played prooncogenic functions in both HER2+ and TNBC cell lines, and in vitro it acted together with the EGF ligand to promote BC proliferation, migration, and invasion. Here, AKT1 is linked to breast cancer.