ArticleBritish journal of cancer2026
Altretamine induces ferroptosis in small cell lung cancer by promoting epigenetic silencing and lysosomal degradation of GPX4.
Article in British journal of cancer, 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
backgroundSmall cell lung cancer (SCLC) is a high-grade and aggressive neuroendocrine carcinoma that remains incurable due to the emergence of drug resistance and frequent relapse. This study aimed to clarify the therapeutic potential and detailed mechanism of altretamine against SCLC.
methodsAltretamine-triggered cytotoxicity and lipid peroxidation were determined by EdU, FerroOrange probes, etc. GPX4 promoter methylation was evaluated by Methylation-specific PCR, chromatin immunoprecipitation, etc. Altretamine-induced GPX4 degradation was examined by bio-layer interferometry, immunoprecipitation, etc.
resultsAltretamine mainly initiates ferroptosis in SCLC cells, accompanied by accumulation of intracellular ROS and lipid peroxidation. Mechanistically, altretamine facilitated the binding of DNMT3A to GPX4 promoter, leading to DNA methylation of GPX4 gene and subsequent transcriptional repression. Moreover, altretamine directly bound to GPX4 protein and accelerated the lysosomal degradation of GPX4 protein in a HSC70-dependent manner. Inhibition of DNA demethylation by inactivating Ten-eleven translocation (TET) proteins synergistically strengthened the anti-SCLC activity of altretamine.
conclusionsOur findings revealed the first time that altretamine induced ferroptotic cell death by promoting DNMT3A-mediated epigenetic silencing of GPX4 gene and HSC70-mediated lysosomal degradation of GPX4 protein in SCLC cells. Altretamine alone or in combination with TET inhibitors is a valuable and credible strategy for the clinical treatment of SCLC.
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