miR-21通过PTEN/PI3K/AKT信号通路调控胶质瘤细胞的增殖

miR-21 Regulates Proliferation of Glioma Cells via PTEN/PI3K/AKT Signal Pathways

探讨miR-21对胶质瘤细胞U87中人第10号染色体缺失的磷酸酶及张力蛋白同源的基因/磷脂酰肌醇3激酶/蛋白激酶B(PTEN/PI3K/AKT)信号通路相关影响作用研究。脂质体Lipofectamine^(TM)2000将miR-21 inhibitor和miR-21 NC转入U87细胞中,48 h后,RT-PCR检测miR-21表达,MTT法检测细胞活力,Annexin V/PI流式双染检测细胞凋亡情况,Western blotting检测PTEN/PI3K/AKT激活情况及程序性细胞死亡因子4(PDCD4),Bax及Bcl-2的表达。与miR-21 NC组比较,miR-21 inhibitor组miR-21表达量显著降低,U87细胞活力下降,细胞凋亡率提高,PI3K、Bcl-2及p-AKT表达量下调,PTEN、PDCD4及Bax表达量上调,差异均具有统计学意义(p<0.01)。miR-21inhibitor能显著的抑制U87细胞的增殖,与PTEN/PI3K/AKT信号通路有关。

To explore effect ofmiR-21 on PTEN/PI3K/AKT signal pathway in glioma cell U87, miR-155 inhibitor and miR-21 NC were transfected into U87 cell by liposome LipofectamineTM2000. After 48 hours, cell viability was measured by MTT assay; Cell apoptosis was measured by flow cytometry; the expression of Bax, Bcl-2, programmed cell death 4 （PDCD4） and phosphatase and tensin homologue deleted on chromosome 10 （PTEN）/ phosphatidylinositol 3 kinase （PI3K）/protein kinase B （AKT） signal pathway related protein was detected by Western blotting. Compared with miR-21 NC group, in miR-21 inhibitor group, the expression of miR-21 was significantly reduced, cell viability of U87 was reduced, cell apoptotic rate was increased, the expression of PI3K, Bcl 2 and p-AKT was decreased, the expression ofPTEN, PDCD4 and Bax was increased, and the differences were significant （p 〈0.01）. miR-21 inhibitor could evidently inhibit the proliferation of U87 cells, which was in relation to PTEN/PI3K/AKT signal pathway.