Effects of IFN beta treatment on gene expression in human fibrosarcoma HT1080 cells. 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. Overall design: RNA sequencing analysis was conducted on HT1080 cells following a 24-hour IFNβ treatment period, with untreated cells serving as controls

环鸟苷酸-腺苷酸合酶（cyclic GMP-AMP synthase, cGAS）-干扰素基因刺激蛋白（stimulator of interferon genes, STING）通路是一种胞质DNA感知系统。该通路的产物干扰素-β（IFNβ）可抑制肿瘤细胞生长，但铁死亡（ferroptosis）是否参与IFNβ诱导的细胞死亡仍不明确。本研究发现，IFNβ可升高肿瘤细胞内的Fe²+水平并增强脂质过氧化程度，同时降低细胞内谷胱甘肽（GSH）的含量。RNA测序（RNA sequencing）数据显示，在经IFNβ处理24小时的HT1080细胞中，铁死亡相关基因的转录表达出现异常，TRIM21、PML、PARP9、PARP14及PARP10等多个基因均呈现上调趋势。上述结果表明，铁死亡参与了IFNβ诱导的肿瘤细胞铁死亡。整体实验设计：对经IFNβ处理24小时的HT1080细胞开展RNA测序分析，以未处理的细胞作为对照。