长非编码RNA FENDRR通过自发MicroRNA-424促进血管瘤内皮细胞的发展

IF 0.1 4区 生物学 Q4 GENETICS & HEREDITY
Qiang Liu
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引用次数: 0

摘要

本研究探讨了FENDRR和miR-424在调节HemECs进展中的作用。利用RT-qPCR检测到FENDRR在HemECs中上调。FENDRR基因的下调抑制了HemECs的活力、迁移和侵袭能力,但加速了细胞的凋亡。此外,MMP-9和VEGFA也受到抑制。随后,荧光素酶报告基因测试证实,HemECs中的miR-424被FENDRR擦拭,并在HemECs中下调。此外,过表达的FENDRR抑制了miR-424模拟物诱导的miR-424高表达。此外,fendr过表达也能逆转miR424模拟物引起的HemECs活力、侵袭性和迁移能力的抑制以及细胞凋亡的增加。此外,通过过表达的FENDRR, mir -424诱导的低MMP-9和VEGFA得以恢复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long Noncoding RNA FENDRR Facilitates Progressions of Hemangioma Endothelial Cells via Sponging MicroRNA-424
The present study investigated effects of FENDRR and miR-424 on modulating HemECs progressions. Using RT-qPCR, FENDRR was detected to be upregulated in HemECs. The knockdown of FENDRR inhibited HemECs viability, migratory and invasive abilities but accelerated the cell apoptosis. Additionally, MMP-9 and VEGFA were also suppressed. Luciferase reporter test then verified that miR-424 in HemECs was sponged by FENDRR and downregulated in HemECs. Furthermore, overexpressed FENDRR restrained miR-424 mimics-induced high miR-424 expression. Beyond that, suppressed HemECs viability, invasiveness and migratory ability and increased apoptosis caused by miR424 mimics were also reversed by FENDRR overexpression. Moreover, miR-424-induced low MMP-9 and VEGFA were restored by overexpressed FENDRR.
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