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Updated: May 17, 2025

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Published on: June 17, 2014
Effects of the carcinogen TCDD on δ-catenin stability and tumorigenic potential in prostate cancer cells
Yue Niu1, Hyoung Jae Lee1,2, Zhiwei Chen1
1College of Pharmacy and Research Institute of Pharmaceutical Sciences, Chonnam National University Gwangju 61186, Republic of Korea.
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.
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