miR-140-5p inhibits the proliferation, migration and invasion of vascular smooth muscle cells by suppressing the expression of NCKAP1

被引:7
|
作者
Ma, Qing [1 ]
Liu, Jiancheng [1 ]
Li, Chunbo [1 ]
Wang, Dong [1 ]
机构
[1] Tangshan Gongren Hosp, Cardiovasc Surg, Tangshan 063000, Hebei, Peoples R China
关键词
aortic dissection; miR-140-5p; NCKAP1; vascular smooth muscle cells; proliferation; invasion; AORTIC DISSECTION; DOWN-REGULATION; CANCER;
D O I
10.5603/FHC.a2021.0003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Introduction. The occurrence of aortic dissection is related to the proliferation and metastasis of vascular smooth muscle cells. In our present study, we found that the expression of miR-140-5p was inhibited in the wall of abdominal aorta of aortic dissection patients. However, the mechanism of miR-140-5p in the development of aortic dissection is unclear. Material and methods. We detected the expression of miR-140-5p and NCK Associated Protein 1 (NCKAP1) in blood vessel of aortic dissection patients and normal people by PCR. Next, we established the miR-140-5p over-expression and miR-140-5p inhibition vascular smooth muscle cells (CRL-1999 cells). The BrdU assays, wound healing assays and transwell assays were performed to detect the proliferation and invasion ability of these cells. Finally, luciferase reporter assay was performed to detect the relationship between miR-140-5p and NCKAP1. Results. The expression of miR-140-5p was suppressed in blood vessel of aortic dissection patients, and the levels of NCKAP1 in those tissues were upregulated. Overexpression of miR-140-5p inhibited the proliferation, migration and invasion of vascular smooth muscle cells. miR-140-5p targeted and suppressed the expression of NCKAP1. Conclusions. miR-140-5p repressed the proliferation, migration and invasion of vascular smooth muscle cells by targeting and inhibiting the expression of NCKAP1. Furthermore, the results of our study suggest new strategies and targets for the clinical treatment of arterial dissection.
引用
收藏
页码:22 / 29
页数:8
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