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迪苏尔菲拉姆/铜在MCF-7细胞中诱导BAK介导的酶独立的亡

Beini Sun¹, Yu Wang¹, Hongce Chen¹

¹MOE Key Laboratory of Laser Life Science & Guangdong Provincial Key Laboratory of Laser Life Science, College of Biophotonics, School of Optoelectronic Science and Engineering, South China Normal University, Guangzhou 510631, China.

The international journal of biochemistry & cell biology

|December 24, 2024

概括

迪苏尔菲拉姆和铜通过增加活性氧物种 (ROS) 和激活诱导亡因子AIF诱导癌细胞死亡. 这种组合疗法向BAK蛋白,促进编程细胞死亡.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
癌症研究癌症研究

背景情况:

与铜 (Cu2+) 结合的二硫 (DSF) 显示出显著的抗癌性质.
底层DSF/Cu2+细胞毒性的精确机制尚未完全阐明.

研究的目的:

研究在MCF-7癌细胞中DSF/Cu2+诱导的亡的分子机制.
确定参与DSF/Cu2+介导细胞死亡的关键蛋白质和途径.

主要方法:

细胞活力测定试验
测量反应性氧物种 (ROS) 水平的测量.
对亡标记物的分析 (染色质凝聚,酸胺外化)
西部涂抹和共同免疫沉.
基因淘汰研究 (AIF,BAK)
活细胞定量光共振能量转移 (FRET) 分析.

主要成果:

DSF/Cu2+治疗增加了细胞内ROS,触发了MCF-7细胞的亡.
亡是由诱导亡因子 (AIF) 从线粒体转移到核的转移介导的,独立于亡酶激活.
AIF的淘汰赛显著降低了DSF/Cu2+细胞毒性.
亲亡蛋白BAK被上调并激活,而BAX没有;BAK淘汰细胞对DSF/Cu2+表现出抵抗力.
DSF/Cu2+破坏了MCL-1和BAK之间的结合,导致BAK的同类寡合化.

结论:

在MCF-7细胞中,DSF/Cu2+会诱导酶独立的亡.
该机制涉及ROS生成,BAK激活和依赖AIF的核转移.
DSF/Cu2+治疗使BAK脱离MCL-1,促进BAK的寡合化和随后的亡.

关键词:

其他AIF的AIF.细胞灭亡 (apoptosis) 是一种死亡的过程.在这里,我们可以看到Bak Bak Bak.它是独立于卡斯帕斯的.迪苏尔菲拉姆/铜

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