ArticleRedox biology2026
Redox-triggered USP18 confers cisplatin resistance in ovarian cancer by selectively activating a non-canonical FSP1-dependent ferroptosis escape pathway.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCisplatin resistance is a primary cause of treatment failure in ovarian cancer (OC), partly due to enhanced antioxidant defenses that counteract cisplatin-induced DNA damage and reactive oxygen species (ROS). Beyond the classic Glutathione Peroxidase 4 (GPX4) pathway, evidence suggests that non-canonical pathways like those mediated by Ferroptosis Suppressor Protein 1 (FSP1) may drive resistance. This study aims to elucidate how such alternative pathways facilitate resistance under cisplatin-induced ROS stress.
methodsUbiquitin Specific Peptidase 18 (USP18) was identified from a deubiquitination library. Protein/RNA interaction and m
resultsCisplatin-induced ROS upregulates the expression of the USP18 through the transcription factor c-JUN, establishing the ROS-c-JUN-USP18 signaling axis. This axis stabilizes the IGF2BP2 protein via USP18-mediated deubiquitination, which in turn enhances the stability of FSP1 mRNA in an m6A methylation-dependent manner, thereby driving the selective activation of the FSP1-mediated pathway over the canonical GPX4 pathway. The predictive efficacy of models derived from the ROS-c-JUN-USP18-IGF2BP2-FSP1 axis was demonstrated by ROC curves and nomograms, confirming their utility in identifying patients with cisplatin-resistant OC. Importantly, the combination of iFSP1 with cisplatin produces a significant synergistic effect, effectively overcoming drug resistance in USP18-high tumors.
conclusionThis study elucidates the mechanism by which the ROS-c-JUN-USP18-IGF2BP2-FSP1 axis regulates cisplatin resistance and proposes a novel iFSP1-cisplatin combination therapy, offering a promising new strategy for OC treatment.
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