ArticleCell death discovery2025
TAZ/NRF2 positive feedback loop contributes to proliferation in bladder cancer through antagonistic ferroptosis.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Tetrastigma Hemsleyanum Polysaccharide Suppresses Triple-Negative Breast Cancer by Disrupting the Hippo-YAP/TEAD4-PDIA4 Axis and Endoplasmic Reticulum Stress Adaptation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PSMD11 stabilizes PGM3 by antagonizing Parkin to promote bladder cancer progression through energy metabolism reprogramming.Cell death & disease · 2026Article
- Article
- Targeting the 5-HTActa pharmacologica Sinica · 2026Article
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- Transcription factor NRF2 and the expression of the Hippo pathway effector TAZ in bladder tumorigenesis are significantly correlated.Discover oncology · 2025Article
- Panobinostat potentiates adagrasib-induced cell death by triggering autophagy in human non-small cell lung cancer.Cell death discovery · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Bladder cancer (BLCA) is a prevalent malignancy characterized by high recurrence and metastasis rates. Emerging evidence suggests that the NRF2-GPX4 axis is closely associated with ferroptosis. The transcriptional coactivator with PDZ-binding motif (TAZ) plays a crucial role in regulating ferroptosis; however, its role in BLCA remains unclear. In our study, we found that TAZ was markedly upregulated in BLCA tissues and BLCA cell lines. Gene set enrichment analysis indicated that TAZ depletion was related to ferroptosis and glutathione metabolism. Our results demonstrated that TAZ promotes the malignant progression of BLCA cells both in vitro and in vivo. Moreover, TAZ enhances NRF2 transcriptional activity through interaction with NRF2. We further revealed that TAZ-TEAD4 regulates NRF2 expression at the transcriptional level. Additionally, NRF2 regulates TAZ transcription by binding to its promoter region, establishing a positive feedback loop between TAZ and NRF2 that sustains GPX4 activation and inhibits ferroptosis in BLCA. These insights provide novel molecular targets for therapeutic treatment in BLCA.
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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.