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在非小细胞肺癌中,EIF4A3诱导的CircDHTKD1通过稳定PFKL来调节糖解

Zhenghua Liu¹, Wenya Li¹, Ziyi Wang¹

¹Department of Thoracic Surgery, The First Hospital of China Medical University, Shenyang, Liaoning, China.

Journal of cellular and molecular medicine

|July 18, 2024

概括

循环DHTDK1 (circDHTKD1) 在非小细胞肺癌 (NSCLC) 中被上调,促进瘤生长和糖解. 这种circRNA通过招募IGF2BP2稳定PFKL,为NSCLC提供潜在的治疗标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

非小细胞肺癌 (NSCLC) 是全球癌症相关死亡的主要原因.
循环RNAs (circRNAs) 在癌症发育中起着重要的作用,在NSCLC中发现有几个被上调.
识别特定的瘤性circRNAs对于开发向疗法至关重要.

研究的目的:

研究circDHTKD1在非小细胞肺癌 (NSCLC) 进展中的作用.
阐明circDHTKD1影响NSCLC细胞表型,瘤生长和糖解的分子机制.
探索circDHTKD1作为NSCLC的治疗点的潜力.

主要方法:

定量实时PCR (RT-qPCR) 用于评估NSCLC组织和细胞中的circDHTKD1水平.
通过RNase R消化和逆转录试验,证实circDHTKD1.1的循环性质.
功能损失和增益测试,以评估circDHTKD1对NSCLC细胞行为和瘤生长的影响.
生物信息学,RIP测试和RNA拉下测试,以确定circDHTKD1,EIF4A3,PFKL和IGF2BP2.2之间的相互作用.
光在位杂交 (FISH) 来确定circDHTKD1亚细胞局部.

主要成果:

发现CircDHTKD1在NSCLC组织和细胞中具有显著的上调,并具有稳定的循环结构.
细胞启动因子4A-III (EIF4A3) 被确定为一个上游调节器,可对NSCLC中circDHTKD1的表达进行上调.
CircDHTKD1促进了NSCLC细胞增殖,瘤生长和糖解.
循环DHTKD1通过升调肝类型的酸果酶-1 (PFKL) 来促进NSCLC的糖解.
CircDHTKD1与胰岛素样生长因子2的mRNA结合蛋白2 (IGF2BP2) 结合,促进PFKL和IGF2BP2之间的相互作用,从而稳定PFKL并增强糖解.

结论:

CircDHTKD1是一种致癌的circRNA,促进NSCLC的进展和糖解.
EIF4A3-circDHTKD1轴在NSCLC的发病过程中起着至关重要的作用.
通过IGF2BP2招募,CircDHTKD1稳定了PFKL,推动了瘤糖解.
准circDHTKD1/IGF2BP2/PFKL通路为NSCLC提供了一个有希望的治疗策略.

关键词:

电路DHTKD1 的情况.欧洲投资基金4A3A3 在IGF2BP2BP2的基础上.这就是为什么PFKL.葡萄糖溶解是什么

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