ArticleBMC cancer2025
Single-cell sequencing combined with urinary multi-omics analysis reveals that the non-invasive biomarker PRDX5 regulates bladder cancer progression through ferroptosis signaling.
Article in BMC cancer, 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.
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Who cites it
2 citing papers in PubMed.
- PRX5 as a critical driver of colorectal cancer stemness and tumorigenicity.Redox report : communications in free radical research · 2026Article
- Multi-omics dissection of fatty acid metabolism heterogeneity identifies PRDX1 as a prognostic marker in bladder cancer.Frontiers in immunology · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
objectiveThis study aimed to elucidate the expression profile and biological implications of peroxidase 5 (PRDX5) in bladder cancer (BC), specifically investigating its influence on BC progression through modulation of reactive oxygen species (ROS) levels and activation of ferroptosis pathways.
methodsWe employed urine proteomics data and transcriptomic information from the Cancer Genome Atlas (TCGA) to identify differentially expressed genes in BC tissues, focusing on PRDX5. Using single-cell RNA sequencing (scRNA-seq), we assessed PRDX5 distribution across various cell types in the tumor microenvironment. We conducted in vitro experiments to analyze the impact of PRDX5 on BC cell proliferation, migration, and invasion, while exploring its mechanisms of modulating ROS levels and ferroptosis. In vivo experiments were performed to observe PRDX5's influence on ferroptosis signaling in tissue contexts.
resultsWe found significant upregulation of PRDX5 in BC tissues, with scRNA-seq revealing its enrichment in bladder epithelial cells, correlating with disease advancement and established BC markers. In vitro analyses showed that overexpressed PRDX5 enhanced proliferation, migration, and invasion of BC cells, while PRDX5 knockout produced opposing effects. Additionally, PRDX5 modulated ROS levels and impacted ferroptosis pathways. In vivo experiments confirmed that PRDX5 knockout inhibited tumor growth and activated ferroptosis signaling pathways in tissues.
conclusionOur study highlights the elevated expression of PRDX5 in BC and its role in promoting tumor progression through regulation of ROS levels and ferroptosis. PRDX5 may serve as a promising target for BC treatment, supporting further exploration of its potential in clinical applications.
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