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微小RNA-27a通过靶向BTG2抑制多形性胶质母细胞瘤细胞的克隆生长和迁移。

miR‑27a suppresses the clonogenic growth and migration of human glioblastoma multiforme cells by targeting BTG2.

作者信息

Li Wei-Qing, Yu Hong-Yu, Zhong Nan-Zhe, Hou Li-Jun, Li Yi-Ming, He Jin, Liu Hui-Min, Xia Chun-Yan, Lu Yi-Cheng

机构信息

Department of Pathology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China.

Department of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China.

出版信息

Int J Oncol. 2015 Apr;46(4):1601-8. doi: 10.3892/ijo.2015.2843. Epub 2015 Jan 22.

Abstract

miR-27a and BTG2 are implicated in gliomagenesis and glioma progression. However, hitherto, a link between miR-27a and BTG2 in glioma has not been reported. In the present study, we investigated the effects of miR-27a on the proliferation and invasiveness of glioblastoma cells in vitro and in a mouse xenograft model and further studied the relation between miR‑27a expression and its target gene BTG2, which was identified by computation prediction algorithms. Our MTT and clonogenic assays showed that miR-27a overexpression significantly increased the clonogenic growth of glioblastoma U87MG and U251MG cells. The Transwell assays further revealed that miR-27a overexpression markedly increased the number of migrated U87MG and U251MG cells. TargetScan and other prediction algorithms identified BTG2 as a target gene of miR-27a, which was confirmed by EGFP reporter and immunoblotting assays showing an inverse relation between miR-27a expression and endogenous BTG2 expression. BTG2 overexpression also increased the proliferation and invasiveness of glioblastoma cells and BTG2 functioned downstream of miR-27a in modulating the proliferation and migration of glioblastoma cells. In conclusion, miR-27a modulates human glioblastoma growth and invasion by targeting BTG2.

摘要

miR-27a和BTG2与胶质瘤的发生及进展有关。然而,迄今为止,尚未有关于miR-27a与BTG2在胶质瘤中存在关联的报道。在本研究中,我们在体外及小鼠异种移植模型中研究了miR-27a对胶质母细胞瘤细胞增殖和侵袭能力的影响,并进一步研究了miR-27a表达与其通过计算预测算法鉴定的靶基因BTG2之间的关系。我们的MTT和克隆形成试验表明,miR-27a过表达显著增加了胶质母细胞瘤U87MG和U251MG细胞的克隆生长。Transwell试验进一步显示,miR-27a过表达显著增加了U87MG和U251MG细胞的迁移数量。TargetScan和其他预测算法将BTG2鉴定为miR-27a的靶基因,这通过EGFP报告基因和免疫印迹试验得到证实,这些试验表明miR-27a表达与内源性BTG2表达呈负相关。BTG2过表达也增加了胶质母细胞瘤细胞的增殖和侵袭能力,并且BTG2在调节胶质母细胞瘤细胞的增殖和迁移中作用于miR-27a的下游。总之,miR-27a通过靶向BTG2调节人胶质母细胞瘤的生长和侵袭。

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