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来自间歇性缺氧非小细胞肺癌的外体miR-106a-5p增加了瘤恶性瘤

Jie Ren¹, Zhuan Jin¹, Yongjie Huang¹

¹Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Physiological reports

|July 31, 2024

概括

在阻塞性睡眠呼吸暂停中间歇性缺氧促进非小细胞肺癌的进展. 外体miR-106a-5p驱动M2巨细胞的两极分化,增强瘤的生长和转移.

科学领域:

在瘤学瘤学.
睡眠医学睡眠医学
分子生物学分子生物学

背景情况:

阻塞性睡眠呼吸暂停 (OSA) 的特点是间歇性缺氧 (IH),与癌症发展有关.
通过OSA影响非小细胞肺癌 (NSCLC) 的确切机制仍在研究中.

研究的目的:

阐明与OSA相关的IH如何促进NSCLC的进展.
确定外体微RNAs在介导IH对NSCLC和巨细胞两极分化影响中的作用.

主要方法:

NSCLC细胞被暴露在IH或室内空气 (RA) 中,随后进行了外基因组提取和表征.
用外体对巨细胞进行处理,以评估STAT3信号传递,M2极化标记物和对NSCLC恶性瘤的影响.
一个裸体小鼠模型被用来评估外体 miR-106a-5p 对M2巨细胞极化和NSCLC进展的影响.

主要成果:

IH外基因组促进了M2巨细胞的两极分化,增强了NSCLC细胞的增殖,入侵和转移.
微阵列分析显示,IH外体中的miR-106a-5p降低了PTEN的调节,并激活了巨细胞中的STAT3信号,促进了M2极化.
在患有NSCLC和OSA的患者中,外体miR-106a-5p水平与呼吸暂停-呼吸暂停指数 (AHI) 正相关.

结论:

通过IH外体转移的外体miR-106a-5p驱动M2巨细胞极化,有助于NSCLC的进展.
外体体中的miR-106a-5p/PTEN/STAT3轴是IH诱导的NSCLC恶性病的关键调解者.
外体miR-106a-5p是患有同时存在NSCLC和OSA的患者的潜在治疗标.

关键词:

外基因组中的miR-106a-5p.在这里,我们可以使用PTEN.在STAT3中,我们可以使用STAT3.非小细胞肺癌的肺癌.阻塞性睡眠呼吸暂停症是什么

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