Moreover, rapamycin treatment significantly increased the protein levels of E-cadherin and markedly diminished the suppressive effect of FGF2 on E-cadherin protein levels (Fig 4E), indicating that the PI3K/Akt/mTOR pathway is involved in FGF2-induced E-cadherin suppression in ovarian cancer cells. Here, AKT1 is linked to ovarian carcinoma.