ArticleMolecular oncology2024
Glutathione S-transferase omega class 1 (GSTO1)-associated large extracellular vesicles are involved in tumor-associated macrophage-mediated cisplatin resistance in bladder cancer.
Article in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Systematic transcriptomic analysis of UDP-glucuronosyltransferases reveals UGT2B11 as a diagnostic and metabolic marker in hepatocellular carcinoma.BMC cancer · 2026Article
- Drug repurposing targeting miRNA-mRNA networks to mitigate areca nut-induced head and neck cancer.Biomedical journal · 2026Article
- Large extracellular vesicles and blebbisomes in cancer: emerging and translational opportunities highlights.Cell communication and signaling : CCS · 2026Review
- Review
- FTO Suppresses Proliferation and Induces Apoptosis of T98G Glioblastoma Cells via N6-methyladenosine Modification of GSTO1.Neurochemical research · 2025Article
- The clinical impact of galectin-8 in drug resistant breast cancer.Journal of Cancer · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Bladder cancer poses a significant challenge to chemotherapy due to its resistance to cisplatin, especially at advanced stages. Understanding the mechanisms behind cisplatin resistance is crucial for improving cancer therapy. The enzyme glutathione S-transferase omega class 1 (GSTO1) is known to be involved in cisplatin resistance in colon cancer. This study focused on its role in cisplatin resistance in bladder cancer. Our analysis of protein expression in bladder cancer cells stimulated by secretions from tumor-associated macrophages (TAMs) showed a significant increase in GSTO1. This prompted further investigation into the role of GSTO1 in bladder cancer. We found a strong correlation between GSTO1 expression and cisplatin resistance. Mechanistically, GSTO1 triggered the release of large extracellular vesicles (EVs) that promoted cisplatin efflux, thereby reducing cisplatin-DNA adduct formation and enhancing cisplatin resistance. Inhibition of EV release effectively counteracted the cisplatin resistance associated with GSTO1. In conclusion, GSTO1-mediated EV release may contribute to cisplatin resistance caused by TAMs in bladder cancer. Strategies to target GSTO1 could potentially improve the efficacy of cisplatin in treating bladder cancer.
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