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LncRNA XIST通过调节STAT3/PD-L1轴作为对miR-12424的竞争性内源RNA来增强胃癌细胞功能

Gaowa Sharen^1,2, Haoyu Meng^3,4, Lei Zhang⁵

¹Department of Pathology, The Affiliated Hospital of Inner Mongolia Medical University Hohhot, Inner Mongolia, P. R. China.

American journal of cancer research

|May 15, 2025

概括

长非编码RNAXIST通过通过海绵miR-124调节STAT3来促进胃癌 (GC). 针对这种XIST/miR-124/STAT3通路为GC提供了潜在的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
基因规则基因规则

背景情况:

胃癌 (GC) 仍然是一个重大的全球健康挑战.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在癌症发展中的作用.
lncRNA X非活性特异性转录 (XIST) 已涉及各种癌症,但其在GC中的特定作用需要进一步阐明.

研究的目的:

研究lncRNA XIST在胃癌中的功能作用.
阐明XIST影响GC进展的潜在分子机制.
在GC的XIST监管网络中识别潜在的治疗点.

主要方法:

定量实时PCR (RT-qPCR) 和基于细胞的测定 (CCK-8,殖民地形成,流细胞计,Transwell,) 评估了XIST和miR-124的影响.
生物信息学和双露西法酶报告员 (DLR) 测定了XIST,miR-124和STAT3.3之间的相互作用.
西方涂抹和异种移植模型评估了分子变化和体内瘤生长抑制.

主要成果:

在GC组织和细胞系中,XIST被显著上调,miR-124被显著下调.
通过XIST敲除或miR-124过度表达,抑制了GC细胞的增殖,迁移和入侵,同时促进了细胞亡.
XIST直接针对miR-124,调节STAT3表达和PD-1,PD-L1,N-cadherin和MMP9等下游目标,最终抑制了体内瘤的生长.

结论:

通过对miR-124.4的竞争性结合,XIST通过上调STAT3来促进胃癌的进展.
XIST/miR-124/STAT3轴代表了胃癌治疗的有前途的治疗标.
调节这一轴可以为管理GC提供一种新的策略.

关键词:

在 LncRNA XIST 中.在PD-1中使用PD-1.在PD-L1中.在STAT3中,我们可以使用STAT3.生物标志物生物标志物胃癌胃癌是一种胃癌.免疫疗法免疫疗法在 miR-12424 里面.治疗目标是治疗的目标.

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