The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines.

By Sylvia Grille, A. Bellacosa, J. Upson, Andres J Klein-Szanto, F. van Roy, W. Lee‐Kwon, M. Donowitz, P. Tsichlis, L. Larue. Cancer Research, 2003

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TGF-β-induced EMT: mechanisms and implications for fibrotic lung disease (2007, background): “In addition, ILK phosphorylates Akt (24) and glycogen synthase kinase (GSK) (44), both of which have been implicated in EMT in malignant cells and during development, respectively.”
Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. (2004, background): “Activation of Akt by ILK leads to suppression of apoptosis (69,70) and perhaps induction of EMT (71).”
Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “PI3K/Akt signaling pathway activation increases tumor cell invasion and metastasis.(157) Steelman et al.”
The role of epithelial-mesenchymal transition in cancer pathology. (2007, background): “Indeed, Akt phosphorylates and inhibits GSK-3b, thus leading to an increase in both signalling b-catenin and Snail, ultimately promoting EMT.(30,38,39) In addition to activating Akt, PI3K can lead to activation of the Rho family small GTPases that are known to have a prominent role in EMT.”
CD44 splice isoform switching in human and mouse epithelium is essential for epithelial-mesenchymal transition and breast cancer progression. (2011, background): “The PI3K/Akt pathway has been shown to play a critical role in promoting EMT, in part through the downregulation of E-cadherin (26).”