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阿特苏纳酸通过向PRDX1和PRDX2来诱导扩散的大B细胞淋巴瘤细胞中的铁亡

Xiaohui Liu¹, Liyi Zeng¹, Jing Liu¹

¹MOE Key Laboratory of Tumor Molecular Biology and Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, Jinan University, Guangzhou, China.

Cell death & disease

|July 11, 2025

概括

阿特苏纳酸 (ART) 向PRDX1和PRDX2,在扩散型大B细胞淋巴瘤 (DLBCL) 中诱导铁亡. 这一发现揭示了ART的存在.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
生物化学生物化学

背景情况:

扩散性大B细胞淋巴瘤 (DLBCL) 是最常见的非霍奇金淋巴瘤 (NHL),呈现出侵略性生长和不良患者结果.
抗疟疾药物阿特苏纳酸 (ART) 具有抗癌作用,包括通过铁灭诱导抑制DLBCL,但其分子标未知.

研究的目的:

在扩散性大B细胞淋巴瘤 (DLBCL) 细胞中识别阿特苏纳酸 (ART) 的直接分子标.
阐明ART诱导的铁亡的机制,并评估其在DLBCL中的治疗潜力.

主要方法:

小分子拉下测定与液体染色学-并联质谱学 (LC-MS/MS) 结合,以确定潜在的ART标.
生物物理分析包括CETSA,光定位,CD光谱和分子对接,以确认ART-PRDX1/2结合.
基因淘汰和过度表达研究,体外细胞测定和体内异种移植模型在裸体小鼠中.

主要成果:

氧化素1和2 (PRDX1和PRDX2) 被确定为ART在DLBCL细胞中的直接结合伙伴.
证实ART与PRDX1和PRDX2结合,特定的残留物被确定为相互作用的关键.
PRDX1/2 Knockdown模仿了ART的铁灭诱导,而PRDX2的过度表达降低了ART的细胞毒性和ROS产量.
ART选择性地消除了具有高PRDX1表达的DLBCL细胞,并在体内证明有效性,没有观察到毒性.

结论:

阿特苏纳酸 (ART) 与PRDX1和PRDX2直接相互作用,在扩散性大B细胞淋巴瘤 (DLBCL) 中诱导铁.
PRDX1和PRDX2是ART抗DLBCL作用的关键调解者,代表了这种血液性恶性瘤的潜在治疗标.

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