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-β (IFNβ) can inhibit tumor cell growth, but it remains unclear whether ferroptosis is involved in IFNβ-induced cell death. We found that IFNβ can increase intracellular Fe2+ and lipid peroxidation levels while decreasing GSH levels in tumor cells. RNA sequencing data showed that IFNβ 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 IFNβ-induced tumor cell ferroptosis. RNA sequencing analysis was conducted on HT1080 cells following a 24-hour IFNβ treatment period, with untreated cells serving as controls