Expression of Twist invokes Akt signaling pathway and increases the amount of Snail Twist has been demonstrated to stimulate the Akt signaling pathway by inducing the expression of Akt. We tested the phosphorylation of Akt in cells expressing Twist and their corresponding parental cells, to Enzalutamide manufacturer examine perhaps the expression of Twist activates the Akt signaling. We discovered that Akt was activated in Hela and MCF7 cells expressing Twist. Serine/threonine protein kinase GSK 3b, a downstream target of PI3K/Akt, was also observed to be inactivated by phosphorylation at serine 9, although the whole GSK 3b stage remained changed. As GSK 3b could phosphorylate b catenin and result in its proteasome degradation, this result was in keeping with our finding that b catenin was stabilized because of the somewhat reduced degree of phosphorylation. The activation of reduction and Akt of GSK 3b in Twist expressing cells were rather interesting, once we showed previously that GSK 3b is the important kinase regulating the cellular localization of Snail and the protein Posttranslational modification (PTM) balance. To help increase this finding, we analyzed the expression of Snail in these cells. We found that the degree of Snail was notably higher in Twist overexpressing cells than that of parental cells. Together, our suggest that expression of Twist could cause the activation of Akt and the reduction of GSK 3b, which in the stabilization of t catenin and Snail in Hela and MCF7 cells. Inhibition of b catenin and Akt signaling pathways control CD44 expression We confirmed that EMT induced the downregulation of E cadherin and the detachment of b catenin from membrane localization. We further showed that EMT activated Akt and suppressed the function of GSK 3b, which is needed for the stabilization and nuclear translocation of b catenin, and thus in the transcription of CD44. We knocked down the appearance of b catenin or inhibited the Akt pathway by wortmannin in cells, to investigate if the b catenin and Akt pathways were critical selective c-Met inhibitor for that induction of CD44. We discovered that either the knockdown of b catenin expression or even the inhibition of Akt route suppressed the expression of CD44. Inhibition of both pathways may further synergistically suppress the expression of CD44, suggesting the activation of these two pathways is crucial for the preservation of CD44 expression. Discussion In this study, we showed that the expression of Twist induced EMT in MCF7 and Hela cells, and that accompanied the increased stem cell like properties and the upregulation of CD44. We found that the upregulation of CD44 was mediated by the activation of b catenin and Akt pathways in these cells, inhibition of both pathways synergistically suppressed the upregulation of CD44. Our research provides several new insights in to the regulation of EMT and cell differentiation program.