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通过促进S100A9表达,HNRNPL促进肝细胞癌细胞中的铁亡

Lanfang Yang¹, Zhibo Zhang¹, Xiangqing Yao¹

¹Department of Hepatopancreas Biliary, Hernia Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, China; Department of Hepatopancreas Biliary, Hernia Surgery, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, China; First Clinical Medical College, Fujian Medical University, Fuzhou, Fujian 350005, China.

Translational oncology

|February 18, 2024

概括

异质核核核糖核蛋白L (HNRNPL) 通过稳定S100A9mRNA,促进肝细胞癌 (HCC) 的铁化. 这一发现揭示了推动HCC进展的新机制,并提供了潜在的治疗点.

科学领域:

分子瘤学分子瘤学
细胞死亡途径的细胞死亡途径.
癌症生物学癌症生物学

背景情况:

肝细胞癌 (HCC) 是一个主要的全球健康问题,有效的治疗方法有限.
铁死是一种受调节的细胞死亡形式,与癌症的进展和治疗耐药性有关.
特定RNA结合蛋白在调节HCC中铁化中的作用仍然不完全理解.

研究的目的:

调查异质核核核糖核蛋白L (HNRNPL) 对HCC细胞铁亡的影响.
阐明HNRNPL影响铁亡的潜在分子机制.
评估针对HCC的HNRNPL的治疗潜力.

主要方法:

在HCC组织和细胞中分析HNRNPL和S100A9表达.
在体外测试测量细胞活性,活性氧物种 (ROS),铁含量,脂质过氧化 (LPO),甲酸 (MDA) 和谷氨 (GSH) 水平.
RNA免疫沉 (RIP),RNA拉下,以及阿克丁诺米辛D测定以确定HNRNPL-S100A9相互作用和mRNA稳定性.
在裸体小鼠的体内异种移植瘤实验中.

主要成果:

在HCC中,HNRNPL和S100A9显著过度表达.
降低HNRNPL降低了HCC细胞活性,并促进了铁亡标志物 (增加铁,LPO,MDA,ROS;减少GSH,GPX4,SLC7A11).
HNRNPL增强了S100A9mRNA的稳定性和表达;S100A9的过度表达或铁化抑制逆转了HNRNPL的淘汰效应.
在体内,减少HNRNPL表达抑制了瘤生长.

结论:

通过通过RNA结合蛋白 (RBP) 的作用增加S100A9mRNA稳定性和表达,HNRNPL促进HCC细胞中的铁亡.
准HNRNPL代表了肝细胞癌的潜在治疗策略.
这项研究揭示了HCC铁化中的新型调节轴.

关键词:

铁化是铁化的一种.在HNRNPL的基础上,HNRNPL 肝细胞癌是肝细胞癌.在RBP中使用RBP.在RIP中,RIP是指RIP的时间.在S100A9A9中使用.

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