Silencing FAK expression inhibited adenomyosis cell migration in vitro and the expression of EMT‑promoting molecules, suggesting that the FAK/PI3K/AKT signaling pathway may participate in the EMT of endometrial cells in adenomyosis.
Furthermore, PI3K/AKT signaling pathway involved in inducing NR4A expression under decidualization stimuli in hESCs and the level of p(Ser473)-AKT was significantly higher in stroma in endometrium from patients with adenomyosis.