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微小RNA-7-5p通过靶向SATB1抑制胶质母细胞瘤细胞的迁移和侵袭。

miR-7-5p inhibits cell migration and invasion in glioblastoma through targeting SATB1.

作者信息

Yin Chang-You, Kong Wei, Jiang Jing, Xu Hao, Zhao Wei

机构信息

Department of Neurosurgery, Yantai Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China.

Department of Emergency, Yantaishan Hospital, Yantai, Shandong 264001, P.R. China.

出版信息

Oncol Lett. 2019 Feb;17(2):1819-1825. doi: 10.3892/ol.2018.9777. Epub 2018 Nov 28.

Abstract

MicroRNAs (miRNAs/miRs) have been revealed to influence the development and progression of glioblastoma. Although a number of miRNAs are abnormally expressed in glioblastoma it is not clear whether they are a factor associated with glioblastoma pathogenesis. In the present study, miR-7-5p was identified as being aberrantly downregulated in glioblastoma tissues and cell lines. miR-7-5p overexpression significantly decreased the migratory and invasive capacity of the cells, while miR-7-5p silencing had the opposite effect. In addition, a luciferase assay confirmed that special AT rich sequence binding protein 1 (SATB1) was a direct target gene of miR-7-5p in glioblastoma. The overexpression of SATB1 in glioblastoma was revealed to promote cell migration and invasion. In addition, SATB1 overexpression may weaken the inhibitory effect of miR-7-5p on cell migration and invasion. miR-7-5p overexpression reversed the effects of SATB1 on cell migration and invasion in glioblastoma cells. In conclusion, miR-7-5p may be a useful therapeutic target for the diagnosis and treatment of patients with glioblastoma.

摘要

微小RNA(miRNA/miR)已被证实会影响胶质母细胞瘤的发生和发展。尽管许多miRNA在胶质母细胞瘤中异常表达,但它们是否为与胶质母细胞瘤发病机制相关的一个因素尚不清楚。在本研究中,miR-7-5p被鉴定为在胶质母细胞瘤组织和细胞系中异常下调。miR-7-5p过表达显著降低了细胞的迁移和侵袭能力,而miR-7-5p沉默则产生相反的效果。此外,荧光素酶报告基因检测证实,富含AT序列结合蛋白1(SATB1)是胶质母细胞瘤中miR-7-5p的直接靶基因。胶质母细胞瘤中SATB1的过表达被证实可促进细胞迁移和侵袭。此外,SATB1过表达可能会削弱miR-7-5p对细胞迁移和侵袭的抑制作用。miR-7-5p过表达逆转了SATB1对胶质母细胞瘤细胞迁移和侵袭的影响。总之,miR-7-5p可能是胶质母细胞瘤患者诊断和治疗的一个有用的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e83/6341908/da571ee031e4/ol-17-02-1819-g00.jpg

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