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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 investigate the effect of miR-21 on PTEN / PI3K / AKT signaling pathway in human glioma U87 human chromosome 10-deleted phosphatase and tensin homologue gene / phosphatidylinositol 3-kinase / protein kinase B (PTEN / PI3K / AKT) the study. Lipofectamine 2000 was used to transfer miR-21 inhibitor and miR-21 NC into U87 cells. After 48 h, miR-21 expression was detected by RT-PCR. Cell viability was measured by MTT assay. Annexin V / PI flow cytometry The apoptosis of PTEN / PI3K / AKT and the expression of PDCD4, Bax and Bcl-2 were detected by double staining. Compared with the miR-21 NC group, miR-21 expression was significantly decreased in miR-21 inhibitor group, U87 cell viability decreased, apoptosis rate increased, PI3K, Bcl-2 and p-AKT expression decreased, PTEN, PDCD4 and Bax The expression was up-regulated, the differences were statistically significant (p <0.01). miR-21inhibitor can significantly inhibit the proliferation of U87 cells, and the PTEN / PI3K / AKT signaling pathway.