ArticleAmerican journal of cancer research2026
Targeting ferroptosis in gefitinib-resistant HCC827 NSCLC cells using erastin.
Article in American journal of cancer research, 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
Overcoming drug resistance remains essential for improving clinical outcomes in non-small cell lung cancer (NSCLC). This study explores the differential susceptibility of drug-resistant cancer cells, utilizing gefitinib (GEF)-resistant HCC827GR NSCLC cells as a model system. We observed that HCC827GR cells inherently display elevated levels of reactive oxygen species (ROS) and increased expression of ferroptosis-related markers when compared with GEF-sensitive cells. Accordingly, the HCC827GR lineage showed heightened responsiveness to erastin-mediated cytotoxicity, as determined by MTT and soft-agar assays. Our mechanistic investigations established that erastin treatment resulted in non-apoptotic cell death, accompanied by mitochondrial dysfunction and G2/M phase arrest in the cell cycle. In-depth analysis demonstrated that erastin notably raised intracellular iron and ROS concentrations and induced lipid peroxidation. Pretreatment with N-acetyl cysteine (NAC) validated the crucial involvement of ROS, and the use of ferrostatin-1 conclusively verified ferroptosis as the predominant mode of cell death. In summary, GEF-resistant HCC827GR cells exhibit increased sensitivity to erastin-induced ferroptosis compared with the parental line. This distinct vulnerability should be further studied as a potential therapeutic approach for targeting drug-resistant NSCLC.
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