ArticleFrontiers in oncology2025
Bioinformatics and experimental unveiling of TIMP1 as a novel therapeutic target in colorectal cancer ferroptosis.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Dual Roles of TIMP-1 in Cancer: From Protease Inhibition to Cytokine Signaling.Molecular biology reports · 2026Review
- In Vivo Models of Diabetes: Unravelling Molecular Pathways in Metabolic and Skeletal Complications.Biomedicines · 2026Review
- Identification of TIMP1 as a Key Regulator of Ferroptosis in Ulcerative Colitis Through Bioinformatics and Functional Experiments.Gastroenterology research and practice · 2026Article
- Significant correlation between ferroptosis-associated genes and ulcerative colitis: implications for diagnosis and treatment.European journal of medical research · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Introduction: Colorectal cancer (CRC) remains a globally prevalent and lethal malignancy, with ferroptosis emerging as a novel cell death mechanism. This study aimed to elucidate the role of key genes in ferroptosis regulation and their impact on CRC malignancy. Methods: Using bioinformatics and experimental methods, we identified TIMP1 as an oncogene that may promote CRC progression via ferroptosis, a pathway implicated in diverse diseases. TIMP1 expression was analyzed in TCGA CRC datasets and validated using the UALCAN database. Results: TIMP1 was demonstrated as a critical ferroptosis-related gene in CRC, with elevated expression correlating with advanced pathological staging. Immunohistochemistry demonstrated significantly higher TIMP1 levels in CRC tissues compared to healthy controls. Functional assays revealed that TIMP1 knockdown enhanced ferroptosis sensitivity, suppressed CRC cell proliferation and migration, and reduced expression of ferroptosis regulators GPX4 and SLC7A11. Conclusion: These findings indicate that TIMP1 drives CRC malignancy through ferroptosis modulation, positioning TIMP1 as a potential therapeutic target and offering novel insights for CRC-targeted therapies.
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