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删除MiR-150通过在MDSC中调高P-STAT3和ROS来促进肺瘤生长

Anqi Qin¹, Hao Chen¹, Fan Xu¹

¹Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research On Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, 063210, People's Republic of China.

Scientific reports

|April 15, 2025

概括

微RNA-150 (miR-150) 删除通过增加髓质衍生抑制细胞 (MDSC) 来促进肺癌的生长. 抑制STAT3信号有效地减少了缺乏miR-150.0.的MDSC中的瘤生长和活性氧物种 (ROS).

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

肺癌是全球主要的恶性瘤.
骨髓系衍生抑制细胞 (MDSCs) 是肺瘤微环境的关键调节者.
微RNAs (miRNAs) 在调节MDSC功能和瘤进展方面发挥着关键作用.

研究的目的:

调查miR-150在肺瘤的背景下调节MDSCs中的特定作用.
阐明miR-150影响肺瘤生长和MDSC活动的分子机制.

主要方法:

使用miR-150淘汰赛 (KO) 小鼠和LLC细胞接种,建立肺瘤模型.
对MDSC种群,血清细胞因子水平 (IL-6,G-CSF) 和瘤中抑制分子表达的分析.
在试验室中对在miR-150抑制后在MDSC中反应性氧物种 (ROS),IRE1α和P-STAT3表达的评估.
在体内评估STAT3抑制剂对瘤生长和ROS水平在miR-150KO小鼠中的有效性.

主要成果:

miR-150的删除显著促进了肺瘤的生长,并增加了MDSC的透.
消除miR-150导致血清IL-6和G-CSF水平升高,并增强了MDSC抑制功能.
在体外抑制miR-150增加了MDSC中的ROS,IRE1α和P-STAT3表达.
在体内给予STAT3抑制剂显著抑制瘤生长,并减少了miR-150KO小鼠的MDSC中的ROS.

结论:

miR-150的删除通过在MDSC中调高P-STAT3和ROS来促进肺瘤的进展.
STAT3信号传递是一个关键的途径,它调解了miR-150缺乏对MDSC和瘤生长的影响.
向STAT3代表了一种潜在的治疗策略,以抵消肺癌中miR-150损失的前瘤性影响.

关键词:

这就是IRE1α.在MDSC中,MDSC是MDSC.在 MiR- 150 中使用.这就是ROSOS ROS.在STAT3中,我们可以使用STAT3.

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