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Xuejiao Wang¹, Xiaobin Wang¹, Tao Jiang¹

¹Department of Thoracic Surgery, The Second Affiliated Hospital of the Air Force Medical University, Baqiao District, Xinsi Road 569, Xi'an, Shaanxi, China.

Functional & integrative genomics

|August 24, 2023

概括

在非小细胞肺癌 (NSCLC) 中,microRNA-22-3p (miR-22-3p) 降低调控,通过向RAC1.1,抑制瘤细胞迁移和上皮-介质细胞过渡. 这个miR-22-3p/RAC1轴为NSCLC提供了潜在的治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

微RNA-22-3p (miR-22-3p) 在各种癌症中表现出瘤抑制作用.
在非小细胞肺癌 (NSCLC) 中miR-22-3p的特定功能和机制尚不清楚.

研究的目的:

研究NSCLC中miR-22-3p的生物功能和分子机制.
探索miR-22-3p/RAC1轴作为NSCLC的治疗点的潜力.

主要方法:

定量实时PCR (RT-qPCR) 和TCGA数据库分析以评估miR-22-3p表达.
试验室试验评估miR-22-3p对NSCLC细胞迁移和上皮层-介质细胞过渡 (EMT) 的影响.
路西法酶记者测定识别miR-22-3p目标基因,特别调查RAC1.

主要成果:

与正常对照组相比,NSCLC组织和细胞中的miR-22-3p表达显著下降.
较低的miR-22-3p水平与淋巴结转移和较大的瘤大小相关.
过度表达miR-22-3p抑制NSCLC细胞迁移和EMT,而其沉默促进了这些过程.
与RAS相关的C3毒素基质1 (RAC1) 被确定为miR-22-3p的直接标.
miR-22-3p通过降低RAC1的调节抑制了细胞迁移和EMT,而RAC1过度表达可以逆转这一效应.

结论:

在NSCLC中,miR-22-3p作为瘤抑制剂起作用.
该miR-22-3p/RAC1信号通路在调节NSCLC细胞迁移和EMT方面发挥着至关重要的作用.
针对miR-22-3p/RAC1轴为NSCLC干预提供了一个有希望的治疗策略.

关键词:

在EMT中,EMT是EMT.路西法拉斯测试试验肺癌是一种肺癌.移民移民移民在RAC1中,RAC1是指RAC1.在 miR-22-3pp 中使用.

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