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KLF11通过抑制GPX4来调节肺腺癌铁和化学敏感性

Guangyin Zhao¹, Jiaqi Liang¹, Guangyao Shan¹

¹Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.

Communications biology

|May 29, 2023

概括

克鲁佩尔样因子11 (KLF11) 通过抑制GPX4.4促进肺腺癌 (LUAD) 的铁化. 这种机制抑制瘤生长并增强化疗敏感性,为LUAD患者提供了一种新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞死亡研究细胞死亡研究

背景情况:

铁亡,一种受调节的细胞死亡形式,与瘤的进展和抗化学疗法的存在有关.
了解调节铁亡的分子机制对于开发新型癌症疗法至关重要.

研究的目的:

调查克鲁佩尔样因子11 (KLF11) 在肺腺癌 (LUAD) 中的作用及其在铁死中的潜在参与.
阐明KLF11影响LUAD细胞增殖和化疗敏感性的分子途径.

主要方法:

用铁灭诱导剂治疗的LUAD细胞的RNA序列查.
在LUAD细胞中对KLF11的基因表达分析 (过度表达和淘汰).
染色体免疫沉测序 (ChIP-Seq) 和RNA测序 (RNA-Seq) 来识别KLF11的目标.
染色体免疫沉定量PCR (ChIP-qPCR) 和双光酶测定以确认KLF11结合和GPX4的转录调节.
在体外和体内实验,以评估KLF11和GPX4.4的功能影响.

主要成果:

在LUAD细胞中,KLF11的表达被铁灭诱导剂上调.
过度表达KLF11促进了铁,抑制了LUAD细胞增殖,增加了化疗敏感性.
KLF11被确定为GPX4的转录抑制剂,GPX4是铁亡的关键调节剂.
恢复GPX4表达可以抵消KLF11对铁亡,增殖和化学敏感性的影响.
在LUAD组织中降低KLF11表达,与患者存活时间减少相关.

结论:

通过抑制GPX4.4,KLF11通过诱导ferroptosis作为LUAD中的瘤抑制剂.
KLF11增强化疗敏感性,并抑制LUAD细胞的增殖.
KLF11代表了改善LUAD治疗结果的潜在治疗标.

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