Abstract
δ-Catenin is a member of the p120-catenin subfamily of armadillo proteins and is known to be upregulated in prostate cancer, promoting tumorigenesis. Unfortunately, the molecular mechanism underlying this effect remains unclear. The carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been linked to an increased risk of prostate cancer. In this study, we explored the effect of TCDD on δ-catenin in prostate cancer cells. TCDD increased the protein levels of δ-catenin in a dose-dependent manner by enhancing its stability. Moreover, TCDD led to an increase in β-catenin expression but a decrease in E-cadherin levels. Further experiments revealed that TCDD stabilized the expression of δ-catenin by inhibiting its ubiquitination-mediated degradation. Finally, TCDD enhanced the motility and migration ability of prostate cancer cells through δ-catenin. These findings suggest that TCDD plays a role in stabilizing δ-catenin in prostate cancer cells, offering a new perspective on preventing δ-catenin degradation and potentially increasing the predictive value of δ-catenin for prostate cancer.