超级增强剂通过FOXA1调解SLC7A11,以调节前列腺癌中的二硫化

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Zhen Kang^1,2, Bin Lin^1,2, Zhi-Bin Ke^1,2

¹Department of Urology, Urology Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.

Cell death & disease

|December 2, 2025

概括

研究人员发现了一种新的细胞死亡途径,即二硫化,与前列腺癌 (PCa) 进展有关. 针对SE/FOXA1/SLC7A11通路可能为PCa提供新的治疗策略,特别是在低葡萄糖环境中.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

前列腺癌 (PCa) 由于雄激素受体信号传递和瘤微环境变化而带来治疗挑战.
不硫化,一种新的细胞死亡形式,涉及细胞骨崩在葡萄糖剥夺和升高的SLC7A11,提供一个潜在的治疗点.

研究的目的:

通过综合数据分析,在前列腺癌中识别与二硫化相关的基因.
阐明SLC7A11及其调节机制在PCa进展和二硫化症中的作用.

主要方法:

用机器学习对TCGA和GEO数据集进行综合分析,以识别关键基因.
使用SLC7A11过度表达和淘汰细胞系的功能研究.
分子测定包括CUT&Tag,ChIP-seq,光酶测定和CRISPR-Cas9基因编辑.

主要成果:

SLC7A11促进PCa细胞的增殖,迁移和入侵.
在葡萄糖饥饿下SLC7A11的过度表达会诱导二硫化,这可以由BAY-876.药理上触发.
FOXA1被确定为SLC7A11的一个关键的转录调节器,由一个超级增强器 (SE) 驱动在chr14:37583488-37589585.
删除SE显著降低了FOXA1和SLC7A11的表达,从而产生了对二硫化的抗性.

结论:

在PCa中,SE/FOXA1/SLC7A11调节轴对于驱动二硫化和瘤进展至关重要.
针对这种途径,特别是在缺乏葡萄糖的瘤微环境中,代表了前列腺癌的有希望的治疗策略.

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