缺氧模拟剂 CoCl2 处理后 Pink1 对内皮细胞线粒体功能障碍的调节作用。
Regulation by Pink1 on the mitochondrial dysfunction in endothelial cells post the hypoxia mimetic agent CoCl2 treatment.
机构信息
Department of Cardiology, Department of Endocrinology, Department of Radiology; China-Japan Union Hospital of Jilin University, Changchun, China.
出版信息
Eur Rev Med Pharmacol Sci. 2018 Sep;22(17):5704-5711. doi: 10.26355/eurrev_201809_15838.
OBJECTIVE
To explore the role of miR-451a in the migration and invasion of non-small cell lung cancer (NSCLC) cells.
MATERIALS AND METHODS
Quantitative Real time-polymerase chain reaction (qRT-PCR) and Western blot were performed to detect the levels of miR-451a and activating transcription factor 2 (ATF2) in NSCLC. Transwell assay was employed to analyze the migratory and invasive abilities in NSCLC cells. Dual-luciferase reporter assay was applied to confirm the binding condition of miR-451 and its target gene in NSCLC cells.
RESULTS
MiR-451a was downregulated in NSCLC tissues and lung cancer cell lines A549 and NCI-H460, while ATF2 was upregulated. The mRNA level of miR-451a was negatively correlated to ATF2. Additionally, miR-451a regulated cell migration and invasion through targeting ATF2. Furthermore, ATF2 could reverse the inhibitory migration and invasion of A549 cells induced by miR-451a.
CONCLUSIONS
MiR-451a inhibits the migratory and invasive abilities of NSCLC cells through ATF2 regulation. The newly identified miR-451a/ATF2 axis provides a novel insight into the pathogenesis of NSCLC.
目的
探讨微小 RNA-451a（miR-451a）在非小细胞肺癌（NSCLC）细胞迁移和侵袭中的作用。
材料与方法
采用实时定量聚合酶链反应（qRT-PCR）和 Western blot 检测 NSCLC 中 miR-451a 和激活转录因子 2（ATF2）的水平。Transwell 实验分析 NSCLC 细胞的迁移和侵袭能力。双荧光素酶报告基因实验验证 miR-451a 及其在 NSCLC 细胞中的靶基因的结合情况。
结果
miR-451a 在 NSCLC 组织和肺癌细胞系 A549、NCI-H460 中表达下调，而 ATF2 表达上调。miR-451a 的 mRNA 水平与 ATF2 呈负相关。此外，miR-451a 通过靶向 ATF2 调节细胞迁移和侵袭。此外，ATF2 可以逆转 miR-451a 诱导的 A549 细胞迁移和侵袭的抑制作用。
结论
miR-451a 通过调节 ATF2 抑制 NSCLC 细胞的迁移和侵袭能力。新鉴定的 miR-451a/ATF2 轴为 NSCLC 的发病机制提供了新的见解。
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