Metformin inhibits 17β-estradiol-induced epithelial-to- mesenchymal transition via βKlotho-related ERK1/2 signaling and AMPKα signaling in endometrial adenocarcinoma cells

The expression of epithelial phenotype marker protein E-cadherin was gradually decreased, and the expression of the intersti- tial phenotype marker protein N-cadherin was gradually

Our results revealed that overexpression of PAK4 further decreased E-cadherin protein expression and increased fibronectin and vimentin protein expression induced by TGF-β1 in

B: In 231-siRNA-IMP3 cells, real-time PCR analyses showed increased E-cadherin and decreased Slug and vimentin in mRNA levels, compared to the control cells (231-mock and 231-nc)..

The expression of E-cadherin was increased and the expression of N-cadherin was decreased at both mRNA and protein level in the HCC cells transfected with pRK5-A20 compared

Furthermore, Western blotting analysis demonstrated that PNUTS inhibition increased the expression levels of vimentin and N-cadherin while suppressing E-cadherin expression in

Our results also showed that metformin significantly suppressed self-renewal capacity of glioblastoma stem cells (GSCs), and expression of stem cell markers Bmi1, Sox2 and

Overexpression of miR-145 significantly decreased the expression level of FSCN1 protein in docetaxel-resistant LAD cells, whereas downregulation of miR145 led to the

Meanwhile, EMT was reversed in SKOV3 and 3AO cells by downregulation of FSCN1, as shown by increased expression of E-cadherin, decreased expression of N-cadherin and vimentin