Our study elucidates a mechanism of NDRG1-regulated Wnt pathway activation and EMT via affecting TLE2 and β-catenin expression in esophageal cancer cells.
These results suggested that PKCι positively regulated β-catenin through negatively regulated autophagy and depletion of PKCι promoted apoptosis via autophagic degradation of β-catenin in esophageal cancer cells.
The purpose of this study is to test whether inhibition of beta-catenin or overexpression of p53 can decrease survivin expression and render esophageal cancer cells more susceptible to apoptosis.
This study shows that beta-catenin accumulation and nuclear localisation is not indicative of transcriptional activity, and therefore is not supportive of a major role in these oesophageal cancer cells.