Regulation by Pink1 on the mitochondrial dysfunction in endothelial cells post the hypoxia mimetic agent CoCl2 treatment
G.-H. Liu, Y. Wen, P. Yang, G.-F. Liu Department of Cardiology, Department of Endocrinology, Department of Radiology; China-Japan Union Hospital of Jilin University, Changchun, China. yanglping87v@sohu.com
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.
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To cite this article
G.-H. Liu, Y. Wen, P. Yang, G.-F. Liu
Regulation by Pink1 on the mitochondrial dysfunction in endothelial cells post the hypoxia mimetic agent CoCl2 treatment
Eur Rev Med Pharmacol Sci
Year: 2018
Vol. 22 - N. 17
Pages: 5704-5711
DOI: 10.26355/eurrev_201809_15838