ArticleJournal of cellular and molecular medicine2025
Identification of FADS2 as a Contributor of Ferroptosis Escape in Bladder Cancer.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Evolutionary conservation analysis reveals a primordial function of STING as a regulator of lipid metabolism via FADS2.Nature communications · 2026Article
- Stearoyl-CoA desaturase 1 integrates tissue-specific oncogenic pathways into a pan-cancer ferroptosis resistance program.Cell death & disease · 2026Review
- Targeting the lipid desaturation network in cancer: from metabolic plasticity to precision therapeutics.Journal of experimental & clinical cancer research : CR · 2026Review
- The promising arsenal of ferroptosis inducers in bladder cancer.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Identification of FADS2 as a Contributor of Ferroptosis Escape in Bladder Cancer.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Ferroptosis is an iron-dependent form of regulated cell death. Previous research indicates that inducing ferroptosis holds significant promise in cancer therapy, particularly for patients who have failed traditional treatments. However, the presence of a ferroptosis escape mechanism in bladder cancer remains unclear, and the therapeutic potential of ferroptosis induction in this context requires further exploration. In this study, bioinformatics analyses and immunohistochemical staining revealed that FADS2 is aberrantly overexpressed in bladder cancer, with its high expression correlating with poor prognosis. Both in vivo and in vitro experiments, including CCK-8 assays, lipid peroxidation assays, iron measurements and ferroptosis-related gene analyses, demonstrated that silencing FADS2 can trigger ferroptosis in bladder cancer cells. Mechanistically, inhibition of the mTOR pathway and SREBP activity was found to reduce FADS2 expression and promote ferroptosis in bladder cancer. In conclusion, this study identifies a critical gene involved in ferroptosis escape in bladder cancer and suggests that FADS2 could serve as a novel prognostic marker and therapeutic target.
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Registered trials
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