ArticleCellular and molecular life sciences : CMLS2025
Synergistic inhibition of TNBC by USP33 and TAP63 through autophagy and ferroptosis activation.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- USP33 Promotes Lung Adenocarcinoma Brain Metastasis by Inhibiting the K48-Linked Ubiquitination and Degradation of S100A9 and Facilitating Vimentin Secretion.International journal of biological sciences · 2026Article
- Global research status and frontiers on autophagy in triple negative breast cancer (TNBC): a comprehensive bibliometric and visualized analysis.Discover oncology · 2025Article
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Authors and funding
8 authors.
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Abstract
backgroundTriple-negative breast cancer (TNBC) is an aggressive malignancy lacking effective targeted therapies. Given the growing importance of regulated cell death pathways, we investigated the role of USP33 and its interaction with the tumor suppressor TAP63 in modulating ferroptosis and autophagy in TNBC.
methodsAn integrative approach combining bioinformatic screening, in vitro molecular and cellular assays, and in vivo xenograft models was employed to evaluate the USP33-TAP63 axis. Protein interaction and ubiquitination were assessed via co-immunoprecipitation and ubiquitin chain analysis. Ferroptosis and autophagy were monitored using fluorescence probes, electron microscopy, and key biomarkers. Statistical significance was assessed via Student's t-test and ANOVA.
resultsUSP33 was significantly downregulated in TNBC tissues and cell lines, correlating with enhanced proliferation, migration, and epithelial-mesenchymal transition. Mechanistically, USP33 stabilized TAP63 through K48-linked deubiquitination, triggering autophagy and ferroptosis by disrupting mitochondrial function and redox balance. Co-overexpression of USP33 and TAP63 synergistically suppressed tumor growth in vitro and in vivo.
conclusionThe USP33-TAP63 axis acts as a central regulator of autophagy and ferroptosis in TNBC, suppressing tumor progression via oxidative stress-induced cell death. These findings offer mechanistic insight and highlight this axis as a promising target for therapeutic intervention in TNBC.
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