ArticleJournal of translational medicine2025
CHI3L1 mediates radiation resistance in colorectal cancer by inhibiting ferroptosis via the p53/SLC7A11 pathway.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- "Ferroptosis-immune" cycle: Research progress of tumor microenvironment responsive nanomaterials in the treatment of pancreatic cancer.iScience · 2026Review
- Article
- The dual roles of ferroptosis in digestive tract tumors: mechanisms, microenvironment regulation, and therapeutic integration with emphasis on immune interactions.Frontiers in immunology · 2026Review
- The Dual Role of SLC7A11 in Colorectal Cancer Ferroptosis: From Molecular Mechanisms to Therapeutic Opportunities.OncoTargets and therapy · 2026Review
- Decoding the ubiquitin network: molecular mechanisms and therapeutic vulnerabilities for precision radio-sensitization in cancer.Molecular cancer · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundRadiotherapy is a key treatment for colorectal cancer (CRC), particularly rectal cancer; however, many patients are resistant to radiation. While it has been shown that CHI3L1 is associated with CRC progression, its specific function and regulatory mechanisms in radiation resistance remain unclear.
methodsThe levels of CHI3L1 in CRC and normal tissue samples were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. To assess the effects of CHI3L1 on CRC cell proliferative, migratory, and invasive capacities, Cell Counting Kit-8 (CCK-8) and Transwell assays were performed. Radiation resistance in CRC cells with varying CHI3L1 expression levels was evaluated through colony formation assay. Western blot and immunofluorescence analyses were conducted to explore the correlation between CHI3L1 and p53 expression levels. Ferroptosis was assessed by determining reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) concentrations in cells with different CHI3L1 expression levels, and a xenograft mouse model was used to identify the molecular mechanisms of ferroptosis in vivo.
resultsSignificant CHI3L1 upregulated was observed in CRC tissues and was associated with promotion of malignant cell behaviors. The number of colonies in CHI3L1-overexpressing groups was significantly greater than that in the control groups following radiation, indicating increased radiation resistance in the former group. Furthermore, CHI3L1 overexpression was associated with p53 downregulation and elevated p53 ubiquitination. Notably, CHI3L1 inhibited the ferroptosis of CRC cells by suppressing p53 expression through the p53/SLC7A11 signaling pathway.
conclusionsCHI3L1 overexpression promotes the proliferation, migration, invasion, and radiation resistance of CRC cells. Elevated CHI3L1 expression is associated with increased p53 ubiquitination and SLC7A11 upregulation. CHI3L1 promotes radiation resistance by suppressing ferroptosis in CRC cells through the p53/SLC7A11 axis.
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