APSB论文：锌指蛋白p52-ZER6通过增强SLC7A11 mRNA稳定性抵抗肿瘤细胞铁死亡脆弱性

2025-06-04 药学学报 等1家媒体报道 科研进展

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该研究揭示了锌指蛋白p52-ZER6通过增强SLC7A11 mRNA的稳定性，提高肿瘤细胞内谷胱甘肽合成，从而有效清除脂质活性氧自由基，增强结直肠癌细胞对铁死亡的抵抗能力。铁死亡是一种因铁离子代谢失衡导致脂质过氧化而诱发的细胞死亡方式，肿瘤细胞因其“铁成瘾性”特征而对铁死亡敏感。然而，肿瘤细胞通过提高抗氧化防御系统来对抗铁死亡。研究发现mRNA稳定性在调控基因表达中起关键作用，与肿瘤的发生、发展及耐药性密切相关。重庆大学江启慧和吴寿荣团队通过多种实验技术，发现p5Human zinc finger protein p52-ZER6 enhances the stability of SLC7A11 mRNA, a key regulator in ferroptosis, by interacting with DAZAP1. This interaction increases cystine uptake and glutathione synthesis in colorectal cancer cells, thereby enhancing their resistance to ferroptosis. The study provides new insights into the molecular mechanisms of ferroptosis resistance in cancer cells and suggests potential therapeutic targets for anticancer strategies. The findings, published in Acta Pharmaceutica Sinica B, highlight the importance of mRNA stability in tumor biology and offer a promising direction for developing novel anticancer therapies targeting p52-ZER6.（摘要由动脉网AI生成）