ArticleMolecular biology reports2026
Repression of FOSL1 augments ferroptosis to overcome oxaliplatin resistance in colorectal cancer by acting on SRSF2.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Iron Metabolism in the Colorectal Tumor Microenvironment: From Preneoplastic Lesions to Cancer Progression.International journal of molecular sciences · 2026Review
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3 authors.
Funding
Abstract
backgroundChemotherapy resistance, particularly resistance to oxaliplatin, remains a major clinical challenge in the treatment of colorectal cancer (CRC). Ferroptosis, a newly characterized form of regulated cell death, has emerged as a potential mechanism for overcoming chemotherapy resistance. The transcription factor FOSL1 has been implicated in CRC progression and chemoresistance; however, its role in ferroptosis is not well defined.
methodsGene and protein expression levels were assessed by quantitative real-time PCR (qRT-PCR) and western blotting, respectively. Malondialdehyde (MDA), glutathione (GSH), and intracellular iron levels were measured using ELISA. Lipid peroxidation was evaluated using the C11-BODIPY 581/591 probe. Cell viability and cell death were determined by the CCK-8 assay and Calcein-AM/propidium iodide (PI) double staining, respectively. The interaction between FOSL1 and the SRSF2 promoter was examined using dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays.
resultsFOSL1 was significantly overexpressed in CRC tissues and oxaliplatin-resistant CRC cells and was negatively correlated with the ferroptosis-related proteins GPX4, SLC7A11, and FTH1. Silencing of FOSL1 reduced oxaliplatin resistance in CRC cells by promoting ferroptosis. Mechanistically, FOSL1 transcriptionally activated SRSF2 expression. Overexpression of SRSF2 reversed the ferroptosis-promoting and oxaliplatin resistance-suppressing effects induced by FOSL1 knockdown.
conclusionFOSL1 promotes oxaliplatin resistance in CRC by suppressing ferroptosis through the upregulation of SRSF2. Targeting FOSL1 may represent a novel therapeutic strategy to overcome oxaliplatin resistance in colorectal cancer.
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