miR-27a suppresses the clonogenic growth and migration of human glioblastoma multiforme cells by targeting BTG2
miR-27a suppresses the clonogenic growth and migration of human glioblastoma multiforme cells by targeting BTG2
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DOI：
10.3892/ijo.2015.2843
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发表时间：
2015-04-01
影响因子：
5.2
通讯作者：
Lu, Yi-Cheng
中科院分区：
文献类型：
--
作者：
Li, Wei-Qing;Yu, Hong-Yu;Lu, Yi-Cheng
miR-27 a和BTG 2与胶质瘤发生和胶质瘤进展有关。然而，迄今为止，miR-27 a和BTG 2在胶质瘤中的联系尚未报道。在本研究中，我们研究了miR-27 a对胶质母细胞瘤细胞在体外和小鼠异种移植模型中的增殖和侵袭性的影响，并进一步研究了miR-27 a表达与其靶基因BTG 2之间的关系，该基因是通过计算预测算法确定的。我们的MTT和克隆形成实验显示miR-27 a过表达显著增加胶质母细胞瘤U87 MG和U251 MG细胞的克隆形成生长。Transwell检测进一步显示miR-27 a过表达显著增加了迁移的U87 MG和U251 MG细胞的数量。靶扫描和其他预测算法将BTG 2鉴定为miR-27 a的靶基因，这通过EGFP报告基因和免疫印迹测定证实，显示miR-27 a表达和内源性BTG 2表达之间的负相关。BTG 2过表达还增加了胶质母细胞瘤细胞的增殖和侵袭性，并且BTG 2在调节胶质母细胞瘤细胞的增殖和迁移中在miR-27 a的下游起作用。总之，miR-27 a通过靶向BTG 2调节人胶质母细胞瘤的生长和侵袭。
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. Target Scan 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.