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通过脂质过氧化,SBFI26诱导三阴性乳腺癌细胞铁亡

Gang He¹, Yiyuan Zhang¹, Yanjiao Feng¹

¹Key Laboratory of Medicinal and Edible Plants Resources Development of Sichuan Education Department, Sichuan Industrial Institute of Antibiotics, School of Pharmacy, Chengdu University, Chengdu, China.

Journal of cellular and molecular medicine

|March 22, 2024

概括

SBFI26是一种脂肪酸结合蛋白5 (FABP5) 抑制剂,通过铁死诱导乳腺癌细胞死亡. 它增加了铁和脂质过氧化,通过上调促进铁亡的基因来抑制瘤生长.

科学领域:

在瘤学瘤学.
生物化学生化学
分子生物学分子生物学

背景情况:

SBFI26抑制了FABP5并抑制了瘤细胞的增殖和转移.
乳腺癌中SBFI26诱导的铁亡的机制尚不清楚.

研究的目的:

阐明SBFI26在乳腺癌细胞中诱导铁亡的机制.

主要方法:

使用CCK-8试验评估了细胞活力.
用Illumina测序进行了转录组分析,并通过qPCR进行了验证.
蛋白质水平通过西部斑点评估,并测量了MDA,T-SOD,Fe,GSH和GSSG的水平.

主要成果:

SBFI26诱导了时间和剂量依赖的细胞死亡,特别是在MDA-MB-231细胞中.
铁-1,GSH和维生素C减弱了SBFI26的影响,而埃拉斯则没有.
SBFI26增加了细胞内MDA,铁和GSSG,同时降低了T-SOD,T-GSH和GSH.
SBFI26上调调节了促进铁亡的基因 (HMOX1,ALOX12,SAT1,ALOX5,ALOX15,ALOXE3,CHAC1) 并降低了抑制剂NFE2L2.2.
SBFI26导致脂肪酸积累,导致铁过载和脂质过氧化.

结论:

SBFI26有效地诱导乳腺癌细胞中的铁亡.
该机制涉及铁的积累,脂质过氧化,以及关键的铁灭相关基因的调节.
SBFI26显示了作为乳腺癌治疗剂的潜力.

关键词:

在SBFI26中,SBFI26是最重要的.美国TNBC电视台铁性化 (ferroptosis) 是一种脂质过氧化过氧化转录组 (transcriptome) 是一个转录组.

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