ArticleDiscover oncology2025
Ferroptotic resistance involved in PTEN-loss prostate cancer progression.
Article in Discover oncology, 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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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
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Who cites it
2 citing papers in PubMed.
- Network Pharmacology and Molecular Docking ofInternational journal of molecular sciences · 2026Article
- Exploiting Oxidative Stress as Achilles' Heel: From Redox Homeostasis to Ferroptosis in Prostate Cancer.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
4 authors.
Funding
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Abstract
Ferroptosis, a newly recognized form of regulated cell death characterized by iron accumulation and lipid peroxidation, plays a pivotal role in cancer development. Herein, we investigated the mechanisms of ferroptotic resistance mediated by Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) loss in prostate cancer cells. The ferroptosis inducer Erastin was used to evaluate the effects on cell viability, colony formation, and Reactive Oxygen Species (ROS) level in three prostate cancer cell lines: PTEN wild-type (DU145 cells) and two of the PTEN null cells (PC3 and LNCaP cells). DU145 cells were prone to ferroptosis, whereas PC3 and LNCaP cells exhibited reduced sensitivity to Erastin-induced ferroptosis. Mechanistically, PTEN loss increased Glutathione peroxidase 4 (GPX4) expression and subsequently decreased intracellular ROS level, which was associated with elevated GPX4 mRNA levels. Knockdown of GPX4 by RNAi reversed the resistance of PTEN-deficient PC3 and LNCaP cells to Erastin. Collectively, our findings suggest that ferroptosis can serve as a potential therapeutic strategy for prostate cancer, and PTEN status may influence cellular sensitivity to ferroptosis.
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