IFNβ drives ferroptosis through elevating TRIM22 and promotes the cytotoxicity of RSL3.

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Tác giả: Qiuyan Chen, Huiyue Dong, Rong Lin, Pengyang Liu, Jun Lu, Jingjing Sun, Zongyang Yu, Huajing Zeng, Wei Zhang, Ling Zhu

Ngôn ngữ: eng

Ký hiệu phân loại: 922.945 *Hindus

Thông tin xuất bản: Switzerland : Frontiers in immunology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 471287

BACKGROUND: Cyclic GMP-AMP synthase (cGAS)-stimulator-of-interferon genes (STING) pathway is a cytosolic DNA sensor system. The production of this pathway, interferon-β (IFNβ), could suppress the growth of tumor cells, yet it is unclear whether ferroptosis is involved in IFNβ-induced cell death. METHODS: The effects of IFNβ on ferroptosis were analyzed in HT1080, 4T1, HCT116 and 786-O cells. HT1080 and 4T1 cells treated with IFNβ were subjected to RNA-Seq analysis. STAT1, STAT3, TRIM21, and TRIM22 were silenced by siRNAs to examine their effects on IFNβ-induced ferroptosis. The cGAS-STING signaling pathway-activated mice were used to evaluate the effects of IFNβ on ferroptosis RESULTS: Here, we found that IFNβ could promote intracellular Fe CONCLUSIONS: Our work reveals a role for IFNβ in promoting ferroptosis and provides evidence that IFNβ could be used with RSL3 to increase cytotoxic effects in tumor cells.
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