GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327198/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327198GEOGSEfalseTamarixetin induces ferroptotic stress through the SLC7A11–GPX4 axis and triggers a compensatory NRF2 responseFerroptosis has emerged as a therapeutic vulnerability in hepatocellular carcinoma, but its interplay with antioxidant defense remains incompletely understood. Here, we investigated whether Tamarixetin induces ferroptotic stress in hepatoma cells and how nuclear factor erythroid 2-related factor 2 (NRF2) signaling responds to this process. Tamarixetin selectively reduced hepatoma cell viability, increased lipid peroxidation, and these effects were partially rescued by ferrostatin-1. Transcriptome analysis revealed enrichment of ferroptosis- and glutathione metabolism-related pathways, highlighting redox-associated genes centered on the SLC7A11–glutathione peroxidase 4 (GPX4) axis. Tamarixetin also increased NRF2 target gene expression, indicating activation of a compensatory antioxidant response to oxidative stress. Molecular docking further suggested a potential interaction between Tamarixetin and the xCT transporter. These findings identify Tamarixetin as a modulator of ferroptotic stress in hepatoma cells and support redox-targeting strategies for liver cancer.2026/05/11GSE327198GSM9651172GSM9651171GSM9651170GSM9651169GSM9651168GSM965116730173327198Homo sapiens