ArticleAmerican journal of cancer research2025
Effects of the carcinogen TCDD on δ-catenin stability and tumorigenic potential in prostate cancer cells.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Computational prioritization of candidate TCDD-associated targets in retinoblastoma using network toxicology and transcriptomic analysis.Frontiers in genetics · 2026Article
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5 authors.
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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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