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通过抑制MAPK/ERK通路,PRDX1 Knockdown促进了埃拉斯诱导的铁亡,并阻碍了扩散大B细胞淋巴瘤的发展

Chuanming Lin^1,2, Shuiling Xie¹, Menger Wang³

¹Department of Hematology, First Affiliated Hospital of Gannan Medical University, No. 128, Jinling Road, Economic Development District, Ganzhou City, Jiangxi Province, 341000, China.

|April 30, 2025

概括

击败百氧化素1 (PRDX1) 通过抑制MAPK/ERK通路,增强了扩散性大B细胞淋巴瘤 (DLBCL) 细胞中的铁亡. 这一发现表明PRDX1是DLBCL治疗的潜在治疗标.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子机制的分子机制

背景情况:

扩散性大B细胞淋巴瘤 (DLBCL) 是一种具有攻击性的血液性恶性瘤.
DLBCL细胞对ferroptosis表现出敏感性,ferroptosis是一种受调节的细胞死亡形式.
氧化素1 (PRDX1) 参与了与癌症进展相关的细胞过程.

研究的目的:

调查PRDX1在DLBCL内的铁化中的作用.
阐明PRDX1影响铁和DLBCL进展的分子机制.

主要方法:

在DLBCL组织和细胞中通过生物信息学和qPCR进行PRDX1表达分析.
在体外评估PRDX1对DLBCL细胞增殖,细胞亡,迁移,入侵和铁亡的影响.
使用异种移植瘤模型进行体内验证.
转录组测序以识别PRDX1-介导的通路和MAPK/ERK通路调制使用异构素.

主要成果:

在DLBCL中,PRDX1的表达是上调的.
降低PRDX1抑制DLBCL细胞的增殖,迁移,入侵和瘤生长,同时促进细胞亡.
PRDX1倒置增强了埃拉斯诱导的铁亡,以增加的铁和MDA表示,并降低了GSH,COX2,GPX4和SLC7A11蛋白水平.
抑制PRDX1降低了MAPK/ERK通路的酸化,这种效应被阿尼索米辛逆转.

结论:

通过抑制MAPK/ERK通路,PRDX1敲除促进铁亡并阻碍DLBCL的进展.
向PRDX1代表了DLBCL的潜在治疗策略.

关键词:

扩散大的B细胞淋巴瘤.铁化是铁化的一种.在MAPK/ERK路径中.过氧素 1 过氧素 1

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