ArticleNPJ breast cancer2025
TRIM39-mediated deubiquitination upregulates RNF168 to evade autophagy-ferroptosis in triple-negative breast cancer.
Article in NPJ breast cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Nanoparticle-Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple-Negative Breast Cancer by Modulating RAB7A Ubiquitination-Associated Stability and Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deubiquitinases at the crossroads of ferroptosis and cancer therapy: mechanisms and therapeutic potential.Molecular biology reports · 2026Review
- Global evolution of ferroptosis research: a comprehensive bibliometric analysis of publication trends, geographic patterns, pharmacological innovation, and translational progress from inception through 2025.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, and due to the lack of robust therapeutic targets, treatment options remain limited to conventional cytotoxic chemotherapy and surgical resection. Autophagy, a lysosome-dependent degradation process, is typically regarded as a survival mechanism. However, excessive degradation of ferritin may indirectly lead to Fe²⁺ accumulation, thereby facilitating ferroptosis. In this study, we reveal for the first time the existence of a TRIM39-RNF168 ubiquitination axis in the TNBC model that targets autophagy-dependent ferroptosis in TNBC cells. The high expression of TRIM39 in TNBC cells confers resistance to ferroptosis and enhances cell survival. Regulation of the TRIM39-RNF168 axis, achieved by knocking down TRIM39 or RNF168, can activate autophagy-coupled ferroptosis in TNBC cells. The activated autophagy-ferroptosis pathway effectively suppresses TNBC progression in vivo, presenting a promising potential therapeutic approach.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.