ArticleCell death & disease2025
CLDN6 triggers NRF2-mediated ferroptosis through recruiting DLG1/PBK complex in breast cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Gene expression profiling identifies ferroptosis-related genes and pathways in human colon cancers cell lines.Frontiers in molecular biosciences · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously identified CLDN6 as a pivotal tumor suppressor in breast cancer and unexpectedly discovered that overexpression of CLDN6 resulted in characteristic ultrastructural alterations of ferroptosis. However, the exact mechanism by which CLDN6 triggers ferroptosis is still elusive in breast cancer. Our study showed that CLDN6 was associated with ferroptosis in breast cancer patients. The integration of CLDN6 and ferroptosis demonstrated remarkable predictive prognostic performance. We observed that CLDN6 triggers NRF2-mediated ferroptosis in vitro and in vivo. Mechanistically, CLDN6 enhanced nuclear export of NRF2 by regulating the PBK-dependent AKT/GSK3β/FYN axis. Further CLDN6 recruited PBK to the cell membrane through the endosomal pathway and bound with the DLG1/PBK complex, thereby promoted the degradation of PBK by the UPS. This study elucidates the previously unrecognized mechanism of CLDN6 triggering NRF2-mediated ferroptosis through recruiting DLG1/PBK complex. This study provides a reliable biomarker for predicting prognosis and is anticipated to guide the selection of therapies targeting ferroptosis in breast cancer.
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