Effects of IFN beta treatment on gene expression in human fibrosarcoma HT1080 cells

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a cytosolic DNA sensing system. The pathway product interferon-ß (IFNß) can inhibit tumor cell growth, but it remains unclear whether ferroptosis is involved in IFNß-induced cell death. We found that IFNß can increase intracellular Fe2+ and lipid peroxidation levels while decreasing GSH levels in tumor cells. RNA sequencing data showed that IFNß caused abnormal transcriptional expression of ferroptosis-related genes in HT1080 cells, with upregulation of multiple genes including TRIM21, PML, PARP9, PARP14, and PARP10. These results indicate that ferroptosis is involved in IFNß-induced tumor cell ferroptosis. Overall design: RNA sequencing analysis was conducted on HT1080 cells following a 24-hour IFNß treatment period, with untreated cells serving as controls