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聚菲林I通过ERK/DNMT1/ACSL4轴诱导割抵抗性前列腺癌细胞中的铁亡

Peiliang Zou^1,2, Zheng Chen¹, Qixiong He²

¹Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, China.

|September 26, 2023

概括

聚林I (PPI) 通过向ERK/DNMT1/ACSL4通路,诱导割抵抗性前列腺癌 (CRPC) 细胞中的铁亡. 这表明PPI是CRPC的有希望的新型治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

雌激素剥夺疗法 (ADT) 后,化抵抗性前列腺癌 (CRPC) 是一个主要的挑战.
迫切需要CRPC的新型治疗策略.
聚林I (PPI) 是来自巴黎多的类固醇素,具有抗癌性质.

研究的目的:

研究PPI在CRPC细胞铁亡中的作用.
在CRPC中阐明PPI诱导的铁亡的潜在分子机制.

主要方法:

西部斑点和RT-qPCR用于分析蛋白质和mRNA表达.
细胞活力测定 (CCK-8) 和铁亡标记分析 (ROS,MDA,Fe2+,GSH).
染色体免疫沉 (ChIP) 和甲基化特异性PCR (MSP) 来评估基因调控.
在体内研究使用裸体小鼠异种移植模型.

主要成果:

PPI抑制了CRPC细胞增殖和诱导铁亡,由改变的GSH,GPX4,MDA,Fe2+和ROS水平证明.
通过抑制DNMT1,PPI抑制了ACSL4促进物甲基化,这种过程通过ERK抑制而逆转.
通过ACSL4调节,DNMT1的敲除促进了铁亡.
在体内,PPI抑制了CRPC瘤的生长.

结论:

PPI通过ERK/DNMT1/ACSL4信号轴作为CRPC细胞中的铁灭诱导剂.
PPI代表了治疗CRPC的潜在新疗法策略.

关键词:

在 ACSL4 中使用.在 DNMT1 中,DNMT1 的值是:埃尔克·埃尔克是什么意思多种类型 I 多种类型 I 割抵抗性前列腺癌是什么铁性化 (ferroptosis) 是一种

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